Abstract
Background
Alzheimer’s disease (AD) is a major cause of disability in older adults and is frequently accompanied by sarcopenia and functional decline, contributing to loss of independence. To investigate the effects of an eight-week combined exercise program on physical and cognitive function, sarcopenia-related outcomes and nutritional status in institutionalized older adults with and without AD.
Methods
Twenty-three participants aged ≥ 65 years (12 with moderate AD and 11 cognitively healthy controls) completed supervised combined aerobic and resistance exercise three times per week for eight weeks. Muscle strength, physical performance, nutritional status, cognition, and activities of daily living were assessed before and after the intervention. Sarcopenia status was classified according to Working Group on Sarcopenia in Older People 2018 (EWGSOP2) criteria using strength and gait speed measures.
Results
Comparison of quadriceps muscle strength before and after exercise showed significant improvement in both Alzheimer's patients (p = 0.013) and the healthy group (p < 0.001). Significant improvement was found in MNA values after exercise in Alzheimer's patients (p = 0.021) and in instrumental activities of daily living in healthy individuals (p = 0.002). After the intervention, quadriceps strength improved significantly in both groups (p < 0.001). When the relationships between parameters were examined, it was found that the relationships between physical function and daily living activities were significant in individuals with Alzheimer's disease (p < 0.05).
Conclusions
Short-term combined exercise is a versatile intervention method applicable to improve muscle strength, mobility, and nutritional status in older adults living in institutions, including those with Alzheimer's disease.
Keyword: Alzheimer’s disease, Sarcopenia, Combined exercise, Nutritional status, Physical performance
Key summary points
Aim
To examine whether an eight-week combined exercise program improves functional and sarcopenia-related outcomes in institutionalized older adults with and without Alzheimer’s disease.
Findings
Combined exercise significantly increased lower limb strength in both groups and improved nutritional status and mobility particularly in participants with Alzheimer’s disease. Functional gains were more pronounced in non-sarcopenic individuals.
Message
Combined exercise is a feasible, low-cost intervention in long-term care that may help counteract sarcopenia-related decline and support functional independence even in older adults with Alzheimer’s disease.
Introduction
Aging is accompanied by progressive physiological, environmental, social, and psychological changes, including declines in muscle mass and strength, disturbances in energy metabolism, malnutrition, and cognitive impairment. Among these age-related conditions, sarcopenia-defined by the loss of muscle mass, muscle strength, and physical performance-has been consistently associated with reduced functional independence, poorer quality of life, and increased mortality in older adults [1, 2].
Alzheimer’s disease (AD), the most common neurodegenerative disorder in later life, frequently coexists with physical inactivity, impaired nutritional intake, and functional decline, all of which may contribute to the development and progression of sarcopenia [3, 4]. Cognitive impairment in AD can adversely affect eating behaviors through diminished hunger perception, difficulties with food access and intake, and impaired taste and olfactory recognition. Consequently, older adults with AD are at increased risk of malnutrition, which has been associated with unfavorable cognitive and functional outcomes [5, 6]. These findings suggest that cognitive impairment, malnutrition, and sarcopenia often coexist and may interact to exacerbate age-related disability. Importantly, sarcopenia extends beyond a decline in physical capacity and is increasingly recognized as a systemic condition that may interact with nutritional status, inflammatory processes, and cognitive health. Skeletal muscle functions as an endocrine organ through the secretion of myokines, which have been implicated in neuroplasticity and synaptic function within the muscle–brain axis. Several mechanisms, including altered myokine signaling, mitochondrial dysfunction, insulin resistance, and chronic low-grade inflammation, have been proposed to link sarcopenia with cognitive health, although the strength and clinical relevance of these associations remain under investigation [7, 8].
Exercise is widely recognized as an effective non-pharmacological intervention to mitigate age-related declines in physical function. Regular physical activity, particularly combined aerobic and resistance exercise, has been shown to improve muscle strength, physical performance, and functional capacity in older adults [9]. In addition to its musculoskeletal benefits, exercise has been associated with favorable effects on cognitive health and may contribute to maintaining independence and quality of life in individuals with dementia. Emerging evidence suggests that interactions within the muscle–brain axis may partly explain these benefits, although the underlying mechanisms are not yet fully understood [5, 10–12].
Despite increasing evidence supporting the benefits of exercise, clinical studies simultaneously evaluating muscular, nutritional, and cognitive outcomes in older adults with AD remain limited. Furthermore, it is not fully understood whether older adults with AD exhibit responses to exercise that differ from those observed in cognitively healthy older adults. Addressing this knowledge gap may provide important insights for developing targeted exercise strategies aimed at preserving functional capacity and overall health in this vulnerable population [13].
Therefore, this study investigated the effects of an eight-week combined aerobic and resistance exercise program on muscle strength, physical performance, cognitive function, nutritional status, activities of daily living, and sarcopenia-related outcomes in older adults with and without Alzheimer’s disease. The primary aim was to determine whether older adults with Alzheimer’s disease demonstrate distinct physiological and cognitive responses to structured exercise compared with cognitively healthy controls.
Methods
Study setting and study population
This quasi-experimental intervention study included two pre-defined groups: older adults with Alzheimer's disease and cognitively healthy older adults. Group allocation was based on participants' existing cognitive status rather than random assignment. Both groups participated in the same supervised combined exercise programme; therefore, comparisons were performed between cognitively healthy older adults and participants with Alzheimer's disease rather than between exercise and non-exercise conditions. First, permission was obtained from the Municipal Health Affairs Directorate to which the nursing home is affiliated. This study was conducted between May 9, 2019, and May 9, 2020, with elderly residents of a municipal care home in Eskişehir, Türkiye. Participant recruitment, baseline and follow-up assessments, and the supervised exercise programme were completed before March 2020. The reporting of the study followed the CONSORT 2010 statement where applicable, and the completed checklist is provided as supplementary material. The study was conducted in accordance with the principles of the Declaration of Helsinki. Ethical approval was obtained from the Eskisehir Osmangazi University Clinical Research Ethics Committee (Approval No: 31, Date: 24 December 2018). Written informed consent was obtained from all participants and/or their legal guardians prior to participation. Participants were informed of their right to withdraw from the study at any time without consequences. All data were collected and stored confidentially and used solely for research purposes.
This study is part of a larger research project conducted at the same municipal facilities. The dataset consists of a total of 23 elderly adults, 12 with AD and 11 healthy. The present analysis is based on a dataset comprising 23 older adults (12 with AD and 11 cognitively healthy controls). The previous publication examined the effects of exercise on functional, cognitive, nutritional, and biochemical parameters. This study focuses on how physical functions, nutrition, activities of daily living, and indicators related to sarcopenia [muscle strength, physical performance, walking speed] are affected by exercise in individuals with Alzheimer's disease [14]. Although both publications originate from the same research project, they address different research questions and outcome measures. Therefore, no duplication of analyses or scientific reporting has occurred.
For participants diagnosed with AD, consent was obtained from both the individual and their legal guardian. As this was a quasi-experimental investigator-initiated study and was not prospectively registered as a clinical trial, no clinical trial registration number is available. Inclusion criteria for the AD group were age ≥ 65 years, a confirmed diagnosis of moderate-stage AD under neurological supervision, and medical clearance for exercise participation. Healthy controls were required to be aged ≥ 65 years, free from any dementia diagnosis, independent in activities of daily living, and medically eligible for exercise. Participants were excluded if they were under 65 years of age, declined participation, or had conditions that could compromise safety or study integrity, including active cancer or cancer history, severe cardiovascular disease, or interruption of exercise participation exceeding two consecutive weeks.
To minimize variability related to disease severity, the AD group included only patients in the moderate stage, all under neurologist supervision. Initially, 24 individuals with AD and 31 healthy older adults were enrolled. In the AD group, withdrawals occurred due to hospitalisation (n = 2), falls (n = 1), influenza infection (n = 4), and prolonged absence from exercise sessions (> 2 weeks, n = 5), resulting in 12 completers. In the control group, exclusions were due to institutional departure (n = 2), injury (n = 1), hospitalisation (n = 2), relocation (n = 2), and voluntary withdrawal (n = 3), leaving 11 participants. Overall, 23 participants (12 with Alzheimer's disease and 11 cognitively healthy older adults) completed the eight-week intervention and were included in the final analyses (Fig. 1).
Fig. 1.
CONSORT 2025 flow diagram
Assessments
Data were collected using a survey form containing demographic information of individuals, standard scales, and measurement methods. Nutritional status was evaluated using the Mini Nutritional Assessment (MNA), a globally validated instrument with proven reliability in Turkish populations [15, 16]. Cognitive function was assessed with the Standardized Mini-Mental State Examination (SMMSE) [17]. Functional independence in daily living was determined using the Barthel Index and the Lawton Instrumental Activities of Daily Living Scale [18].
Lower extremity strength was quantified using a PowerTrack Manual Muscle Tester by assessing maximal isometric quadriceps force of the dominant limb. Participants sat at the edge of a bed with knees positioned at 90° flexion and performed knee extension against standardized resistance until force generation could no longer be sustained. After familiarization, three trials were completed with three-minute rest intervals, and the mean value was calculated [19]. Handgrip strength, as an indicator of upper limb muscle strength, was measured using a Jamar Hand Dynamometer (90 kg). Participants were seated without arm support, with the elbow maintained at 90° flexion, and were instructed to exert maximal grip force. Three measurements were obtained with one-minute rest intervals, and the mean value was used for statistical analyses [20].
Physical performance was assessed using the 10-Meter Walk Test (10MWT) and the Timed Up and Go (TUG) test [21]. TUG completion times were classified based on commonly used clinical cut-off values, with < 10 s representing normal mobility, < 20 s indicating functional independence, 20–29 s reflecting variable mobility, and ≥ 30 s suggesting impaired mobility [22, 23]. Both tests were repeated three times, and mean scores were calculated for subsequent analyses.
Given the lack of access to body composition measurement tools (BIA or DXA) and legal limitations on transferring institutionalised participants to hospital settings, sarcopenia status was determined in accordance with the EWGSOP2 (2019) consensus framework using muscle strength and physical performance measures. Handgrip strength and gait speed were used as the primary indicators for classification [2, 24]. Participants in both groups were subdivided into subgroups based on probable sarcopenia, sarcopenia, or no sarcopenia. Because the number of participants within each sarcopenia category was limited, subgroup analyses within the Alzheimer's disease and cognitively healthy groups were not statistically feasible. Therefore, participants were analysed collectively when examining the associations between sarcopenia status and other study variables.
All participants completed an eight-week combined exercise programme performed three times per week. Exercise sessions were conducted in groups, with cognitively healthy older adults and participants with Alzheimer's disease attending separate sessions. Each session was led by the researcher, a licensed physiotherapist, while two additional physiotherapists attended the sessions to ensure participant safety and monitor the correct execution of the exercises. Prior to programme initiation, medical clearance was obtained from an internal medicine specialist, and a follow-up medical evaluation was conducted at week five to monitor participant safety throughout the intervention. Participants were instructed to maintain their habitual dietary intake, daily activities, and physical activity patterns throughout the study period. No structured dietary intervention was implemented, and nutritional intake was not formally monitored or recorded during the study. Therefore, dietary modifications were unlikely to have systematically influenced the observed findings; however, because nutritional intake was not formally assessed, their potential contribution cannot be completely excluded.
Each exercise session lasted approximately 60 min and consisted of a warm-up (10 min), aerobic training (30 min), resistance exercises (10 min), and a cool-down period (10 min). Lower limb resistance training was prescribed according to the one-repetition maximum (1-RM) principle using sandbags, whereas upper limb strengthening exercises were performed using therabands with progressively increasing resistance (Table 1). Exercise intensity was individualized using the Borg Rating of Perceived Exertion Scale, with participants encouraged to maintain a moderate intensity level [25].
Table 1.
Summary of the eight-week combined exercise programme
| Component | Description |
|---|---|
| Intervention duration | 8 weeks |
| Frequency | 3 sessions/week |
| Supervision | One researcher physiotherapist and two observer physiotherapists per session |
| Session duration | Approximately 60 min |
| Warm-up | 10 min |
| Aerobic training | 30 min |
| Resistance training | 10 min |
| Cool-down | 10 min |
| Session organization | Group sessions with separate groups for cognitively healthy older adults and participants with Alzheimer's disease |
| Lower extremity exercises | Sandbag exercises based on the 1-RM principle |
| Upper extremity exercises | Theraband exercises with progressively increasing resistance |
| Intensity | Moderate intensity according to Borg Rating of Perceived Exertion Scale |
| Initial workload | Approximately 60% of maximal heart rate |
| Progression | Heart rate target increased by ~ 5% every two weeks; resistance adjusted by increasing external load and band tension |
| Safety measures/monitoring | Assessment of vital signs before each session; Continuous monitoring of exercise performance and participant safety throughout each session |
| Adaptations during intervention | Exercise intensity reduced or sessions terminated in case of pain, respiratory distress, excessive sweating, changes in skin colour, or abnormal vital signs |
| Withdrawal criterion | Absence from exercise sessions for more than two consecutive weeks |
The exercise programme was implemented in accordance with World Health Organization recommendations for physical activity in older adults. Sessions commenced at approximately 60% of maximal heart rate, and exercise intensity was increased by approximately 5% every two weeks according to heart rate responses, perceived exertion, and individual tolerance. Resistance progression was achieved by adjusting external load and theraband tension over time. Vital signs were assessed before each session, and participants were continuously monitored for signs of exercise intolerance, including excessive sweating, changes in skin colour, respiratory distress, pain, or abnormal physiological responses. When necessary, exercise intensity was reduced, additional rest periods were provided, or sessions were terminated to ensure participant safety. Participants presenting with abnormal baseline vital signs were not permitted to exercise on that day. Individuals who missed more than two consecutive weeks of sessions were withdrawn from the programme.
All outcome measures were reassessed following completion of the intervention, and pre-post changes and relationships among key variables were subsequently analysed. During the study period, no additional rehabilitation programme, structured physical activity intervention, or nutritional intervention was introduced beyond the supervised exercise sessions described in the study protocol. Participants continued to receive their routine institutional care.
Statistical analysis
Continuous variables were expressed as mean ± standard deviation, while ordinal variables were presented as median (25th-75th percentile). Normality was assessed using the Kolmogorov–Smirnov and Shapiro–Wilk tests. Between-group differences were analyzed using the Kruskal–Wallis test for non-parametric data and independent samples t-test for normally distributed variables. Within-group comparisons were performed using paired samples t-test or Wilcoxon signed-rank test as appropriate. For variables not meeting normality assumptions, relationships were examined using Spearman’s correlation coefficient. A p-value < 0.05 was considered statistically significant. All analyses were conducted using IBM SPSS Statistics version 21 (SPSS Inc., Chicago, IL, USA).
Results
Changes before and after exercise in healthy and AD participants
Participants sosyo-demographic charecteristics and pre-post intervention outcomes for the AD and control groups are summarised in Table 2. With the exception of serum vitamin D, cognitively healthy participants demonstrated consistently better baseline and follow-up values across all measures. However, after the exercise programme, improvements in nutritional status and functional mobility in the AD group attenuated the initial between-group differences.
Table 2.
Comparison of cognitive status, daily activities, nutrition, and functional status before and after exercise in healthy older adults and those with Alzheimer’s disease
| Parameters | Group | N | Before exercise | After exercise | ||||
|---|---|---|---|---|---|---|---|---|
| Mean ± Std. deviation |
Median (25%−75%) |
P | Mean ± Std. deviation |
Median (25%−75%) |
P | |||
| Age | Healthy | 11 | 77,91 ± 7,52 | 76 (73–85) | 0,899 * | |||
| Patient | 12 | 78,42 ± 10,97 | 81 (70,25,87,50) | |||||
| BMI | Healthy | 11 | 28,33 ± 3,55 | 27,34 (24,93–31,25) | 0,864* | |||
| Patient | 12 | 25,08 ± 3,84 | 24,35 (21,95- 27,39) | |||||
| SMMT | Healthy | 11 | 22.45 ± 4.97 | 22.00 (20.00–25.00) | < 0.001* | 24.26 ± 4.08 | 25.00 (24.00–27.00) | < 0.001* |
| Patient | 12 | 11.26 ± 5.45 | 12.00 (8.75–13.75) | 12.59 ± 4.46 | 12.00 (9.25–14.75) | |||
| ADL | Healthy | 10 | 3.61 ± 8.44 | 0.00 (0.00–4.25) | 0.004** | 0.28 ± 0.90 | 0.00 (0.00–0.00) | < 0.001** |
| Patient | 11 | 9.01 ± 4.75 | 8.00 (6.00–11.00) | 5.93 ± 1.24 | 6.00 (5.25–6.75) | |||
| EADL | Healthy a | 10 | 7.21 ± 3.99 | 7.00 (5.25–8.00) | < 0.001** | 0.01 ± 0.00 | 0.00 (0.00–0.00) | 0.009** |
| Patient | 11 | 0.83 ± 1.25 | 0.00 (0.00–2.00) | 0.93 ± 1.08 | 0.50 (0.00–2.00) | |||
| MNA | Healthy | 11 | 18.78 ± 8.39 | 22.00 (19.50–22.50) | 0.006 ** | 23.01 ± 2.70 | 23.00 (22.00–25.50) | 0.095* |
| Patient b | 11 | 12.78 ± 7.88 | 16.50 (1.00–18.00) | 21.05 ± 2.67 | 21.75 (18.38–23.25) | |||
| Time to walk | Healthy | 11 | 10.10 ± 4.61 | 8.37 (8.05–9.29) | 0.045** | 8.48 ± 2.03 | 7.97 (6.55–10.37) | < 0.001* |
| Patient | 12 | 10.94 ± 2.66 | 9.85 (9.36–11.94) | 11.71 ± 1.82 | 11.68 (10.75–12.18) | |||
| TUG | Healthy | 11 | 11.24 ± 5.93 | 9.80 (7.84–10.61) | 0.052** | 9.86 ± 3.21 | 8.59 (7.45–11.81) | 0.338* |
| Patient | 12 | 12.58 ± 3.25 | 11.81 (11.50–13.27) | 10.92 ± 1.88 | 10.55 (9.41–12.64) | |||
| DQMS | Healthy c | 11 | 10.64 ± 2.31 | 11.30 (8.20–12.70) | 0.224* | 23.80 ± 8.75 | 26.00 (13.60–32.00) | < 0.001* |
| Patient d | 12 | 9.33 ± 1.41 | 9.50 (8.43–9.50) | 10.69 ± 1.40 | 10.40 (9.33–11.80) | |||
| DGS | Healthy | 11 | 16.00 ± 7.39 | 15.00 (8.50–22.75) | < 0.001* | 26.64 ± 6.19 | 27.00 (24.00–32.00) | 0.003* |
| Patient | 12 | 14.83 ± 5.59 | 14.00 (11.25–19.75 | 17.33 ± 6.85 | 18.00 (10.25–22.75) | |||
SMMT Standardized Mini Mental Test, ADL Activity of Daily Living, EADL Instrumental Activity of Daily Living, MNA Mini Nutritional Assessment, DQMS Dominant Quadriceps Muscle Strength, DGS Dominant Grip Strength
*Independent Samples T Test, mean ± Std. Deviation
**Mann–Whitney Rank Sum Test, Median (25%−75%)
a: Comparison of Instrumental Daily of Living Activity in healthies before and after exercise (p = 0.002)
b: Comparison of MNA in Alzheimer's patients before and after exercise (p = 0.021)
c: Comparison of Quadriceps muscle Strength in Health before and after exercise (p < 0.001)
d: Comparison of Quadriceps muscle strength in Alzheimer's patients before and after exercise (p = 0.013)
In the AD group, MNA scores increased significantly, indicating improved nutritional status (p = 0.021). Quadriceps strength also showed a significant post-intervention gain (p = 0.013), supporting a favourable effect on sarcopenia-related muscle function. Although performance outcomes improved, these changes were not statistically significant. In healthy older adults, significant improvements were observed in quadriceps strength (p < 0.001) and instrumental activities of daily living (p = 0.002). Other parameters, including gait speed, grip strength, cognitive scores, and functional performance, showed non-significant positive trends. Importantly, mean TUG performance improved to below the 10-s threshold for normal mobility, suggesting a clinically relevant enhancement in functional capacity.
Pre- post differences based on the presence of sarcopenia
According to the multiple variance analysis between subgroups, differences were found between the presence/absence of sarcopenia and physical functions both before and after exercise. However, no differences were found in the comparison of MNA, SMMT, ADL, and EADL scores among the subgroups. Moreover, non-sarcopenic individuals exhibited significantly higher handgrip strength and better mobility performance, characterised by shorter 10 m walk and TUG completion times, compared with participants with sarcopenia (Table 3).
Table 3.
Pre-study differences between groups according to the presence of sarcopenia
| Pre-exercises assessments | Groups | N | Min | Max | Mean | Std. dev | Median | Q1 | Q3 | P |
|---|---|---|---|---|---|---|---|---|---|---|
| Age (year) | 1 | 5 | 65.00 | 76.00 | 71.20 | 4.55 | 73.00 | 68.00 | 74.00 |
0.017 (1–2) |
| 2 | 16 | 55.00 | 92.00 | 81.13 | 9.37 | 82.50 | 79.00 | 89.00 | ||
| 3 | 2 | 68.00 | 76.00 | 72.00 | 5.66 | 72.00 | 68.00 | 76.00 | ||
| BMI (kg/m2) | 1 | 5 | 24.14 | 31.25 | 26.18 | 2.90 | 24.93 | 24.68 | 25.91 |
0.486 (NS) |
| 2 | 16 | 21.08 | 34.72 | 26.34 | 4.23 | 25.89 | 22.80 | 28.86 | ||
| 3 | 2 | 26.99 | 33.31 | 30.15 | 4.47 | 30.15 | 26.99 | 33.31 | ||
| Grip Strength (kg) | 1 | 5 | 18.00 | 33.00 | 26.60 | 5.81 | 28.00 | 24.00 | 30.00 |
0.012 (2–3), (1–2, 2–3)a |
| 2 | 16 | 8.00 | 29.00 | 18.75 | 6.79 | 19.00 | 14.00 | 24.00 | ||
| 3 | 2 | 32.00 | 36.00 | 34.00 | 2.83 | 34.00 | 32.00 | 36.00 | ||
| 10 m walking time | 1 | 5 | 7.13 | 15.03 | 9.51 | 3.16 | 8.30 | 8.05 | 9.03 |
0.024 (2–3),(2–3)a |
| 2 | 16 | 8.23 | 23.40 | 11.24 | 3.86 | 9.75 | 9.18 | 11.91 | ||
| 3 | 2 | 7.39 | 7.64 | 7.52 | 0.18 | 7.52 | 7.39 | 7.64 | ||
| DQMS | 1 | 5 | 7.30 | 13.60 | 9.90 | 2.55 | 9,10 | 8.20 | 11.30 |
0.110 (Ns), (2–3)a |
| 2 | 16 | 7.30 | 12.20 | 9.60 | 1.61 | 9.50 | 8.40 | 10.40 | ||
| 3 | 2 | 12.70 | 13.20 | 12.95 | 0.35 | 12.95 | 12.70 | 13.20 | ||
| TUG | 1 | 5 | 7.78 | 19.12 | 11.07 | 4.58 | 9.42 | 8.95 | 10.07 |
0.026 (2–3), (2–3)a |
| 2 | 16 | 7.84 | 28.08 | 12.82 | 4.69 | 11.58 | 10.57 | 13.26 | ||
| 3 | 2 | 6.42 | 7.77 | 7.10 | 0.95 | 7.10 | 6.42 | 7.77 | ||
| SMMT | 1 | 5 | 2.00 | 25.00 | 15.80 | 9.42 | 18.00 | 11.00 | 23.00 |
0.714 (Ns) |
| 2 | 16 | 2.00 | 30.00 | 16.19 | 7.46 | 13.50 | 12.00 | 22.00 | ||
| 3 | 2 | 20.00 | 22.00 | 21.00 | 1.41 | 21.00 | 20.00 | 22.00 | ||
| ADL | 1 | 5 | 0.00 | 21.00 | 5.00 | 9.11 | 0.00 | 0.00 | 4.00 |
0.134 (Ns) |
| 2 | 14 | 0.00 | 27.00 | 7.86 | 6.60 | 7.00 | 4.00 | 10.00 | ||
| 3 | 2 | 0.00 | 0.00 | 0.00 | 0.00 | 0.00 | 0.00 | 0.00 | ||
| EADL | 1 | 5 | 0.00 | 8.00 | 4.80 | 3.27 | 6.00 | 3.00 | 7.00 |
0.071 (Ns) |
| 2 | 14 | 0.00 | 8.00 | 2.36 | 2.92 | 1.50 | 0.00 | 3.00 | ||
| 3 | 2 | 7.00 | 17.00 | 12.00 | 7.07 | 12.00 | 7.00 | 17.00 | ||
| MNA | 1 | 5 | 4.00 | 21.50 | 16.40 | 7.22 | 18.00 | 17.00 | 21.50 |
0.246 (Ns) |
| 2 | 16 | 0.00 | 26.50 | 13.91 | 9.53 | 17.00 | 1.50 | 20.75 | ||
| 3 | 2 | 22.00 | 22.50 | 22.25 | 0.35 | 22.25 | 22.00 | 22.50 |
Kruskal -Wallis One Way Analysis of Variance on Ranks, According to ESWOPs Group 1: Probable Sarcopenia, Group 2: Sarcopenia, Group 3: No- Sarcopenia, a: Differences between groups after exercise intervention according to the presence of sarcopenia
P Pairwise Comparisons, Min Minimum, Max Maximum, DQMS Dominant Quadriceps Muscle Strength, TUG The timed Up & Go test, SMMT Standardized Mini Mental Test, ADL Activity of Daily Living, EADL Instrumental Activity of Daily Living, MNA Mini Nutritional Assessment, N.S Not significant
After the eight-week exercise program, significant differences were observed between groups based on sarcopenia status. Participants with sarcopenia exhibited lower grip strength compared to the other two groups (Group 1: 27,83 ± 4,40; Group2: 15,86 ± 6,15; Group 3: 37,33 ± 5,77, p = 0.001). Significant between-group differences were found in 10-m walking time (11.49 ± 1.81 vs. 6.47 ± 0.24 s; p = 0.004), dominant quadriceps strength (13.20 ± 5.98 vs. 29.67 ± 4.93; p = 0.016), and TUG performance (11.50 ± 2.55 vs. 7.46 ± 1.05 s; p = 0.011), favouring the non-sarcopenic group (Table 3).
Analysis of sarcopenia-related parameters according to EWGSOP2 cut-off values demonstrated that, in the healthy group, both gait speed (M:1.00 ± 0.51 m/sn; F: 1.04 ± 0.29 m/sn) and grip strength (M: 29.89 ± 7.59 kg; F: 20.00 ± 5.66 kg) reached normal ranges (gait speed ≥ 0,8 m/sn, grip strength M: 30 kg; F:20 kg) for both sexes. In the AD groups, it was observed that there was an improvement in all measured values after eight weeks of exercise treatment, but grip strength remained below the normal value (M: 21.20 ± 7.01 kg; F: 12.29 ± 5.35 kg) (Table 4).
Table 4.
Distribution of strength and performance in groups by gender
| Group | Parameters | Male | Female | Cut off value * |
|---|---|---|---|---|
| Mean ± Std. deviation | Mean ± Std. deviation | |||
| Healthy people (9 Male, 2 Female) | BMI | 28.05 ± 3.80 | 29.99 ± 1.79 | F: 17, M: 24 |
| Gait Speed Before | 0.82 ± 0.19 | 0.99 ± 0.28 | < 0.8 m/s | |
| Gait Speed After | 1.00 ± 0.51 | 1.04 ± 0.29 | ||
| TUG- Before | 11.17 ± 6.50 | 11.53 ± 3.65 | ≥ 20 s | |
| TUG- After | 9.76 ± 3.47 | 10.32 ± 2.48 | ||
| D. Quadriceps -B | 10.69 ± 2.54 | 10.40 ± 1.27 | ||
| D. Quadriceps -A | 26.23 ± 7.67 | 12.84 ± 1.08 | ||
| Grip Strength -B | 28.33 ± 4.87 | 19.00 ± 7.07 |
< 20 kg F < 30 kg M |
|
| Grip Strength -A | 29.89 ± 7.59 | 20.00 ± 5.66 | ||
| Alzheimer people (5 Male, 7 Female) | BMI | 24.79 ± 2.57 | 27.89 ± 4.30 | F: 17, M: 24 |
| Gait Speed Before | 1.16 ±.22 | 1.05 ± 0.31 | < 0.8 m/s | |
| Gait Speed After | 1.17 ±.06 | 1.16 ± 0.24 | ||
| TUG- Before | 13.00 ± 3.75 | 12.28 ± 3.11 | ≥ 20 s | |
| TUG- After | 11.22 ± 2.35 | 10.71 ± 1.64 | ||
| D. Quadriceps -B | 10.14 ± 1.59 | 8.76 ± 1.01 | ||
| D. Quadriceps -A | 11.78 ± 1.04 | 9.91 ± 1.09 | ||
| Grip Strength -B | 21.80 ± 6.09 | 14.14 ± 5.73 |
< 20 kg F < 30 kg M |
|
| Grip Strength -A | 21.20 ± 7.01 | 12.29 ± 5.35 |
D. Quadriceps-B Dominant Quadriceps muscle strength before exercises training, D. Quadriceps-A Dominant Quadriceps muscle strength after exercises training
*: Cruz- Jentoft, 2019
Within-group parameter relationships pre- and post-exercise
Associations between muscle strength, physical performance, cognitive status, nutritional level, and independence in daily living were examined for both groups. In the AD group, pre-intervention analysis revealed a significant correlation between walking time and independence in activities of daily living (ADL) (r = 0.651, p = 0.030). Completion time for the TUG test was also associated with ADL (r = 0.001, p = 0.853) and instrumental ADL (EADL) (r = –0.616, p = 0.044). Post-intervention, a positive correlation was observed between quadriceps strength and ADL (r = 0.628), indicating that functional improvements were linked to cognitive and physical integration. This finding supports the muscle–brain axis theory at a clinical level (Table 5).
Table 5.
Examining the relationships between intra-group parameters before and after exercise
| Parameters | Group of Alzheimer's | |||||||
|---|---|---|---|---|---|---|---|---|
| Before exercise training | After exercise training | |||||||
|
MNA R(p) |
SMMT R(p) |
ADL R(p) |
EADL R(p) |
MNA R(p) |
SMMT R(p) |
ADL R(p) |
EADL R(p) |
|
| Time to walk | .19 (.58) | -.10 (.77) | .65 (.03)* | -.37 (.26) | .19 (.56) | .12 (.70) | -.02 (.95) | .46 (.13) |
| TUG | .05 (.90) | -.26 (.43) | .85 (.001)** | -.62 (.04)* | .36 (.26) | .15 (.64) | -.10 (.76) | .28 (.38) |
| Quadriceps strength | -.08 (.83) | .42 (.18) | -.22 (.53) | .47 (.15) | -.18 (.58) | -.35 (.27) | .63 (.03)* | -.23 (.48) |
| Grip strength | -.05 (.88) | -.18 (.58) | .31 (.36) | .32 (.34) | .16 (.62) | -.11 (.74) | .37 (.24) | .19 (.55) |
| Group of healthy | ||||||||
|---|---|---|---|---|---|---|---|---|
| Before exercise training | After exercise training | |||||||
| Time to walk | -.16 (.64) | .02 (.96) | .11 (.76) | -.53 (.12) | -.42 (.19) | -.61 (.05)* | .53 (.09) | - |
| TUG | -.15 (.65) | .03 (.94) | .16 (.67) | -.53 (.11) | -,22 (.51) | -.64 (.04)* | .23 (.50) | - |
| Quadriceps strength | .03 (.92) | -.13 (.70) | .10 (.78) | .35 (.32) | .40 (.23) | .33 (.32) | -.44 (.17) | - |
| Grip strength | .62 (.04)* | .21 (.53) | -.17 (.64) | .63 (.05) | .40 (.22) | .42 (.19) | -.50 (.12) | - |
TUG Timed Up & Go, Test R Spearman Correlation coefficient, SMMT Standardized Mini Mental Test, ADL Activity of Daily Living, EADL Instrumental Activity of Daily Living, MNA Mini Nutritional Assessment
*: p < 0,05
**: p < 0,001
In the healthy group, pre-intervention grip strength was correlated with nutritional status (r = 0.620, p = 0.042). After the exercise program, cognitive function showed significant associations with mobility tests, including walking time and TUG performance (r = –0.609, p = 0.047; r = –0.636, p = 0.035) (Table 5).
Discussion
Alzheimer's disease is a progressive neurodegenerative disorder associated with impairments in cognitive function, nutritional status, muscle health, and physical performance, all of which contribute to reduced functional independence in older adults [4, 13]. In addition, low body mass index (BMI) has been identified as an independent risk factor for cognitive decline and Alzheimer's disease [26], while malnutrition associated with reduced appetite, sensory changes, and impaired self-feeding may accelerate muscle loss and further exacerbate cognitive deterioration [27]. Consequently, sarcopenia is highly prevalent among individuals with neurodegenerative disorders [28]. Against this background, the present study investigated the effects of an eight-week combined exercise programme on muscle strength, physical performance, cognitive function, and nutritional status in institutionalised older adults with Alzheimer's disease and cognitively healthy controls.
Early detection of sarcopenia and implementation of exercise-based interventions in individuals with Alzheimer's disease may have the potential to slow functional decline and support physical independence. Exercise is recognised as a non-pharmacological strategy that may improve muscle strength and endurance while potentially supporting cognitive function through mechanisms proposed in previous studies [29]. Previous studies have proposed that exercise-related increases in BDNF, synaptic connectivity, neurogenesis, and neuronal resilience may contribute to cognitive benefits observed in individuals with Alzheimer's disease [28, 30, 31]. Aerobic and resistance training have also been reported to increase hippocampal volume and may contribute to improvements in memory, learning, executive function, and attention [32, 33]. Additionally, previous studies have suggested that exercise may improve cerebral blood flow, optimize oxygen and glucose utilization, reduce neuroinflammation, and limit oxidative stress [34], thereby providing a plausible biological basis for the cognitive benefits reported in the literature. However, the present study did not directly evaluate these biological mechanisms. Therefore, these pathways should be interpreted as potential explanatory mechanisms rather than findings demonstrated by the current study.
In the present study, participation in the eight-week combined exercise programme was associated with modest improvements in cognitive performance in both participants with Alzheimer's disease and cognitively healthy older adults. The observed changes in MMSE scores may reflect the cognitive engagement associated with repeated participation in structured exercise sessions, although the underlying mechanisms were not directly evaluated in the present study. In addition, the group-based format may have facilitated social interaction and engagement, which have previously been suggested as factors that can indirectly support cognitive function [35]. These findings may be interpreted in the context of the “shared resource hypothesis,” which suggests that motor skills, attention, and executive functions are governed by the same neural networks [36]. The observed association between post-exercise TUG and 10-m walk test performance and cognitive measures is consistent with the reported relationship between physical and cognitive function, although causality cannot be inferred from the present study. MMSE scores in cognitively healthy participants reached the Turkish normative threshold (23/24), suggesting preserved global cognitive performance following the intervention. However, cognitive reserve was not directly assessed and therefore cannot be inferred from the present findings.
Previous studies suggest that regular physical activity may promote neuroplastic changes related to attention and memory, thereby facilitating learning and motor adaptation [34]. Accordingly, exercise is increasingly recognised as a potentially supportive and rehabilitative strategy for individuals with Alzheimer's disease. Overall, the available evidence suggests that exercise interventions may contribute not only to improvements in physical capacity but also to the maintenance of cognitive function. Although the present study was not designed to evaluate disease progression or neuroplasticity directly, the findings, together with previous evidence, suggest the potential value of structured exercise programmes as part of a comprehensive approach to maintaining physical function and supporting cognitive health in older adults with Alzheimer's disease.
In the present study, sarcopenia classification did not differ significantly between participants with Alzheimer's disease and cognitively healthy older adults; therefore, the entire sample was analysed together according to the EWGSOP2 criteria. Participants were categorized as probable sarcopenia, sarcopenia, or no sarcopenia. Although these subgroup analyses should be interpreted cautiously due to the limited sample size, individuals with sarcopenia demonstrated poorer functional performance, including lower grip strength and impaired mobility, as reflected by differences in grip strength, 10-m walk time, and TUG performance. These findings are consistent with previous evidence indicating that sarcopenia is closely associated with reduced muscle strength and physical performance in older adults. Although the exercise programme was associated with improvements in several functional outcomes, differences according to sarcopenia status remained evident after the intervention. The persistence of lower strength and mobility performance among individuals with sarcopenia following eight weeks of exercise may suggest that longer-term or more targeted interventions may be required to achieve comparable functional gains. However, these findings should be interpreted cautiously considering the small sample size and the absence of a non-exercise control group.
After the exercise intervention, participants without sarcopenia demonstrated functional performance values closer to expected ranges, whereas improvements among individuals with sarcopenia were more limited. Although walking speed above 0.8 m/s has been associated with better mobility outcomes and lower risk of adverse functional outcomes in older adults, achieving this threshold after the intervention may indicate clinically meaningful improvement in mobility capacity. However, the findings should be interpreted cautiously, as the present study did not directly assess fall incidence or quality of life outcomes.
Physical inactivity is considered an important contributor to the development and progression of sarcopenia. Resistance, strength, and functional exercise programmes have been shown to improve muscle function and physical performance in older adults. A Cochrane review demonstrated that resistance training can enhance physical performance among older adults [37]. Consistent with this evidence, our study showed improvements in quadriceps strength following the exercise programme, particularly among participants with Alzheimer's disease (p = 0.013). In addition, quadriceps strength was positively associated with activities of daily living (r = 0.628, p = 0.029), suggesting a close relationship between lower-limb muscle function and functional capacity. Cognitively healthy older adults also demonstrated improvements in instrumental activities of daily living and quadriceps strength. Overall, these findings support the importance of maintaining muscle strength as a component of functional health in older adults. The observed improvements in quadriceps and grip strength alongside better TUG and walking performance are consistent with EWGSOP recommendations and previous evidence highlighting the association between muscle function and mobility outcomes [2, 23].
Muscle weakness has been associated with impairments not only in motor performance but also in cognitive domains such as executive function and attention in previous studies [23, 38]. Our findings are consistent with evidence suggesting that sarcopenia may affect both physical and cognitive aspects of ageing. Recent research has highlighted skeletal muscle as a metabolically active tissue capable of producing myokines that may potentially influence brain function [1–4]. The muscle-brain interaction has therefore been proposed as an important framework for understanding the relationship between sarcopenia and neurodegenerative processes. Exercise-induced myokine responses, including potential effects on BDNF and synaptic plasticity, have been suggested as possible mechanisms underlying cognitive benefits; however, these pathways were not directly evaluated in the present study [31]. Therefore, integrated approaches addressing both physical decline and cognitive vulnerability may be valuable for supporting functional health in older adults.
Malnutrition in older adults is associated with adverse outcomes, including increased mortality risk, falls, hospitalization, and loss of functional capacity [39]. This risk may be further increased among individuals with Alzheimer's disease. Previous studies have suggested that inadequate nutritional status may occur during the course of dementia and may serve as an indicator of increased vulnerability [40]. Reported malnutrition prevalence in individuals with Alzheimer's disease varies considerably, with some studies reporting rates between 0% and 23.2%, whereas higher prevalence rates have also been described [41]. In the present study, BMI values were within or above the normal range in both sexes, differing from reports associating lower BMI with Alzheimer's disease. This finding highlights that muscle impairment in Alzheimer's disease may not always be reflected by overall body weight and supports the importance of incorporating functional measures, such as grip strength, gait speed, and balance, into sarcopenia assessment rather than relying solely on anthropometric measures [2].
Although no dietary intervention was implemented and dietary intake was not directly assessed, nutritional screening scores improved after eight weeks of exercise in the Alzheimer's disease group (MNA score, p = 0.021), and baseline differences between groups were no longer observed. These findings suggest that participation in structured exercise may be associated with improved nutritional status indicators; however, the underlying factors contributing to this change remain unclear. Improvements in muscle strength and functional capacity may potentially influence nutritional status through greater participation in daily activities, although this mechanism requires further investigation.
The findings of the present study may be interpreted within the conceptual framework of the “muscle-brain-nutrition triangle,” which highlights the potential interrelationship between physical function, cognitive health, and nutritional status in older adults. Previous research has proposed that exercise-related biological pathways, including myokine signalling, neuroplastic adaptations, and improved muscle function, may contribute to cognitive and functional benefits [3, 5, 12]; however, these mechanisms were not directly evaluated in the current study. In our study, changes in MMSE scores were modest, and improvements observed in participants with Alzheimer’s disease should be interpreted as preliminary findings rather than evidence of disease modification.
The nutritional findings should also be interpreted cautiously. Although nutritional screening scores improved in the Alzheimer’s disease group after the exercise intervention, no dietary intervention was implemented and actual food intake was not assessed. Therefore, the observed improvement may reflect multiple factors, including changes in physical function, participation, or daily engagement. Future studies incorporating objective nutritional assessments and biological markers are needed to further clarify the relationship between exercise, muscle function, cognition, and nutritional status.
Finally, when considered alongside previous literature, the findings of the present study suggest that even relatively short-term, institution-based exercise programmes may contribute to improvements in selected physical and cognitive outcomes among older adults [35, 38, 42]. However, the optimal type, intensity, and duration of exercise remain unclear, and further studies with larger samples, longer intervention periods, and controlled designs are needed to determine the most effective exercise strategies for individuals with and without Alzheimer’s disease.
Limitations
This study has several limitations. First, the relatively small sample size limits the statistical power and generalizability of the findings. The sample size reflects the recruitment process, as participants were recruited from a single institutional care facility and participation was voluntary. Therefore, the findings should be considered preliminary and confirmed in larger, multicentre studies involving more diverse populations. Second, the absence of a non-exercise control group prevents attributing the observed changes exclusively to the exercise intervention. Although routine institutional care remained unchanged during the study period, unmeasured environmental factors, social interaction associated with group-based exercise sessions, and repeated exposure to assessment procedures may have contributed to the observed outcomes. Third, the intervention duration was limited to eight weeks, which may not have been sufficient to capture longer-term adaptations in muscle mass, physical function, or cognitive outcomes. Fourth, sarcopenia was classified according to the EWGSOP2 algorithm, which emphasizes muscle strength and physical performance, because direct measures of muscle mass could not be obtained. This may have affected the precision of sarcopenia classification. Finally, although nutritional screening scores improved, dietary intake was not quantitatively assessed, and therefore the contribution of unmeasured nutritional or environmental factors cannot be excluded. Despite these limitations, the present study provides preliminary evidence regarding the feasibility and potential clinical value of combined exercise interventions for institutionalized older adults, including those with Alzheimer's disease.
Implications for clinical practice
Combined aerobic and resistance exercise programmes may be feasible for integration into routine care in nursing home settings, including among individuals with moderate Alzheimer’s disease. The present findings suggest that structured exercise participation may be associated with improvements in strength, mobility, and nutritional screening outcomes, even within a relatively short intervention period. Therefore, combined exercise may represent a promising multidomain approach to support functional capacity and overall health in vulnerable institutionalized older adults. However, larger controlled studies with longer follow-up periods are required before definitive conclusions regarding its effects on sarcopenia-related disability and independence can be established.
Conclusions
This study highlights the potential relationship between sarcopenia, nutritional status, and cognitive function in institutionalized older adults with and without Alzheimer’s disease. The findings may be interpreted within the framework of the muscle-brain-nutrition interaction, emphasizing the importance of considering physical, nutritional, and cognitive domains together in geriatric care. An eight-week combined exercise programme was associated with improvements in selected measures of muscle strength, mobility, and nutritional screening outcomes, with modest improvements observed in cognitive performance. These preliminary findings suggest that structured exercise is a feasible and promising non-pharmacological approach to support functional health in institutionalized older adults, including those with Alzheimer’s disease. However, given the small sample size, the absence of a non-exercise control group, and the lack of direct assessment of muscle mass, the findings should be interpreted with caution. Larger multicentre controlled studies with longer follow-up periods are needed to confirm these findings and to determine the long-term effects of exercise on sarcopenia progression, cognitive decline, and functional independence.
Acknowledgements
We would like to express our sincere gratitude to lecturer Ahmet Musmul for his support in the statistical design and analysis process of this study.
Authors’ contributions
Conceptualization: Y.K., S.Y.; Methodology: Y.K., S.Y., P.Y.,F.K.; Writing – original draft preparation: Y.K.; Writing-review and editing: Y.K., S.Y., P.Y.; Supervision: Y.K., S.Y. All authors have read and agreed to the published version of the manuscript.
Funding
Not applicable.
Data availability
All data generated or analyzed during this study are available from the corresponding author upon reasonable request.
Declarations
Ethics approval and consent to participate
The study was conducted in accordance with the principles of the Declaration of Helsinki. Ethical approval was obtained from the Eskisehir Osmangazi University Clinical Research Ethics Committee (Approval No: 31, Date: 24 December 2018). Written informed consent was obtained from all participants and/or their legal guardians prior to participation. Participants were informed of their right to withdraw from the study at any time without consequences. All data were collected and stored confidentially and used solely for research purposes.
Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s Note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
References
- 1.Cruz-Jentoft AJ, Landi F, Schneider SM, Zúñiga C, Arai H, Boirie Y, et al. Prevalence of and interventions for sarcopenia in ageing adults: A systematic review. Age Ageing. 2014;43(6):748–59. 10.1093/ageing/afu115. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Cruz-Jentoft AJ, Bahat G, Bauer J, Boirie Y, Bruyère O, Cederholm T, et al. Sarcopenia: revised European consensus on definition and diagnosis. Age Ageing. 2019;48(1):16–31. 10.1093/ageing/afy169. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3.Arosio B, Calvani R, Ferri E, Coelho-Junior HJ, Carandina A, Campanelli F, et al. Sarcopenia and cognitive decline in older adults: targeting the muscle-brain axis. Nutrients. 2023;15(8):1853. 10.3390/nu15081853. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4.Marzetti E, Calvani R, Tosato M, Cesari M, Di Bari M, Cherubini A, et al. Sarcopenia: An overview on current definitions, diagnosis and treatment. Clin Cases Min Bone Metab. 2020;17(1):1–10. 10.11138/ccmbm/2020.17.1.001. [DOI] [Google Scholar]
- 5.Dominguez LJ, Veronese N, Vernuccio L, Catanese G, Inzerillo F, Salemi G, et al. Nutrition, physical activity, and other lifestyle factors in the prevention of cognitive decline and dementia. Nutrients. 2021;13(11):4080. 10.3390/nu13114080. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6.Moretti R, Morelli ME, Caruso P. Vitamin D in neurological diseases: a rationale for a pathogenic impact. Int J Mol Sci. 2018;19(8):2245. 10.3390/ijms19082245. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7.Gomes MJ, Martinez PF, Pagan LU, Damatto RL, Cezar MDM, Lima ARR, et al. Skeletal muscle aging: influence of oxidative stress and physical exercise. Oncotarget. 2017;8(12):20428. 10.18632/oncotarget.14670. [DOI] [PMC free article] [PubMed]
- 8.Peng TC, Chen WL, Wu LW, Chang YW, Kao TW. Sarcopenia and cognitive impairment: A bidirectional relationship and potential mechanisms. Ageing Research Reviews. 2023;88:101964. 10.1016/j.arr.2023.101964. [DOI]
- 9.Lautenschlager NT, Almeida OP. Physical activity and cognition in old age. Curr Opin Psychiatry. 2006;19(2):190–3. 10.1097/01.yco.0000214347.38787.37. [DOI] [PubMed] [Google Scholar]
- 10.Marzola P, Melzer T, Pavesi E, Gil-Mohapel J, Brocardo PS. Exploring the role of neuroplasticity in development, aging, and neurodegeneration. Brain Sci. 2023;13(12):1610. 10.3390/brainsci13121610. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 11.Balion C, Griffith LE, Strifler L, Henderson M, Patterson C, Heckman G, et al. Vitamin D, cognition, and dementia: a systematic review and meta-analysis. Neurology. 2012;79(13):1397–405. 10.1212/WNL.0b013e31826c197f. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 12.Allahverdi H, Faramarzi M. Exercise and brain health in aging: The role of the muscle–brain axis in improving cognitive functions. Sport Physiol. 2024;16(63):94–107. 10.22089/spj.2025.17632.2350. [DOI] [Google Scholar]
- 13.Peng TC, Chen WL, Wu LW, Chang YW, Kao TW. Sarcopenia and cognitive impairment: a systematic review and meta-analysis. Clin Nutr. 2020;39(9):2695–701. 10.1016/j.clnu.2019.12.014. [DOI] [PubMed] [Google Scholar]
- 14.Kar F, Kavlak Y, Yıldız S, Yıldız P, Musmul A, Uslu S. Eight-week exercise program improved the quality of life of Alzheimer’s patients through functional, cognitive, and biochemical parameters. Ir J Med Sci. 2023;192(2):655–63. 10.1007/s11845-022-03029-3. [DOI] [PubMed] [Google Scholar]
- 15.Farooqui K, Khan AA, Paul T, Sirajudeen J, Khan HA, Farooqui FK, et al. Challenges and management strategies in the nutrition of older people with diabetes. J Diabetes Endoc Pract. 2023;6(3):126–33. 10.1055/s-0043-1771201. [DOI] [Google Scholar]
- 16.Saka B. Yaşlı hastalarda malnütrisyon. İç Hastalıkları Dergisi. 2010;17:223–32 (e-ISSN: 3108-3552). [Google Scholar]
- 17.Güngen C. Standardize Mini Mental Test’in Türk toplumunda hafif demans tanısında geçerlik ve güvenilirliği. Turk Psikiyatri Derg. 2002;13(4):273–81. [PubMed] [Google Scholar]
- 18.Mahoney FI, Barthel D. Functional evaluation: the Barthel index. Md State Med J. 1965;14:56–61. [PubMed] [Google Scholar]
- 19.Mentiplay BF, Perraton LG, Bower KJ, Adair B, Pua YH, Williams GP, et al. Assessment of lower limb muscle strength and power using hand-held and fixed dynamometry: a reliability and validity study. PLoS ONE. 2015;10(10):e0140822. 10.1371/journal.pone.0140822. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 20.Bohannon RW. Dynamometer measurements of hand-grip strength predict multiple outcomes. Percept Mot Skills. 2001;93(2):323–8. 10.2466/pms.2001.93.2.323. [DOI] [PubMed] [Google Scholar]
- 21.Shubert TE, Schrodt LA, Mercer VS, Busby-Whitehead J, Giuliani CA. Are scores on balance screening tests associated with mobility in older adults? J Geriatr Phys Ther. 2006;29(1):33–9. [PubMed] [Google Scholar]
- 22.Podsiadlo D, Richardson S. The timed “Up & Go”: a test of basic functional mobility for frail elderly persons. J Am Geriatr Soc. 1991;39(2):142–8. 10.1111/j.1532-5415.1991.tb01616.x. [DOI] [PubMed] [Google Scholar]
- 23.Bohannon RW. Reference values for the Timed Up and Go Test: a descriptive meta-analysis. J Geriatr Phys Ther. 2006;29(2):64–8. [DOI] [PubMed] [Google Scholar]
- 24.Wallengren O, Bosaeus I, Frändin K, Lissner L, Falk Erhag H, Wetterberg H, et al. Comparison of the 2010 and 2019 diagnostic criteria for sarcopenia by the European Working Group on Sarcopenia in Older People (EWGSOP) in two cohorts of Swedish older adults. BMC Geriatr. 2021;21(1):600. 10.1186/s12877-021-02533-y. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 25.Liao CD, Tsauo JY, Wu YT, Huang YC, Lin LF, Huang SW, et al. A review of the components of exercise prescription for sarcopenic older adults. Eur Geriatr Med. 2023;14(5):1155–70. 10.1007/s41999-023-00772-4. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 26.Sobów T, Fendler W, Magierski R. Body mass index and mild cognitive impairment-to-dementia progression in 24 months: a prospective study. Eur J Clin Nutr. 2014;68(11):1216–9. 10.1038/ejcn.2014.167. [DOI] [PubMed] [Google Scholar]
- 27.Pacifico J, Geerlings MA, Reijnierse EM, Phassouliotis C, Lim WK, Maier AB. Prevalence of sarcopenia as a comorbid disease: a systematic review and meta-analysis. Exp Gerontol. 2020;131:110801. 10.1016/j.exger.2019.110801. [DOI] [PubMed] [Google Scholar]
- 28.Chang KV, Hsu TH, Wu WT, Huang KC, Han DS. Association between sarcopenia and cognitive impairment: a systematic review and meta-analysis. J Am Med Dir Assoc. 2016;17(12):1164.e7-1164.e15. 10.1016/j.jamda.2016.09.013. [DOI] [PubMed] [Google Scholar]
- 29.Li X, Ji M, Zhang H, Liu Z, Chai Y, Cheng Q, et al. Non-drug therapies for Alzheimer’s disease: a review. Neurol Ther. 2023;12(1):39–72. 10.1007/s40120-022-00416-x. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 30.Tarumi T, Patel NR, Tomoto T, Pasha E, Khan AM, Kostroske, K.,et al. Aerobic exercise training and neurocognitive function in cognitively normal older adults: a one-year randomized controlled trial. J Internal Med. 2022;292(5):788–803. 10.1111/joim.13534. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 31.Hess NCL, Dieberg G, McFarlane JR, Smart NA. The effect of exercise intervention on cognitive performance in persons at risk of, or with, dementia: A systematic review and meta-analysis. Healthy Aging Res. 2014;3(3):1–10. 10.12715/har.2014.3.3. [DOI] [Google Scholar]
- 32.Li P, He Y, He M. The comprehensive impact of exercise interventions on cognitive function and quality of life in Alzheimer’s disease patients: a systematic review and meta-analysis. BMC Geriatr. 2025;25(1):871. 10.1186/s12877-025-06454-y. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 33.Xu L, Gu H, Cai X, Zhang Y, Hou X, Yu J, et al. The effects of exercise for cognitive function in older adults: a systematic review and meta-analysis of randomized controlled trials. Int J Environ Res Public Health. 2023;20(2):1088. 10.3390/ijerph20021088. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 34.Kirk-Sanchez NJ, McGough EL. Physical exercise and cognitive performance in the elderly: current perspectives. Clin Interv Aging. 2014;9:51–62. 10.2147/CIA.S39506. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 35.Clark DJ, Manini TM, Ferris DP, Hass CJ, Brumback BA, Cruz-Almeida Y, et al. Multimodal imaging of brain activity to investigate walking and mobility decline in older adults (mind in motion study): hypothesis, theory, and methods. Front Aging Neurosci. 2020;11:358. 10.3389/fnagi.2019.00358. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 36.Gillespie LD, Robertson MC, Gillespie WJ, et al. Interventions for preventing falls in older people living in the community. Cochrane Database Syst Rev. 2012;9:CD007146. 10.1002/14651858.CD007146.pub3. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 37.Kim J, Suh SI, Park YJ, Kang M, Chung SJ, Lee ES, et al. Sarcopenia is a predictor for Alzheimer’s continuum and related clinical outcomes. Sci Rep. 2024;14(1):21074. 10.1038/s41598-024-62918-y. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 38.Stillman CM, Esteban-Cornejo I, Brown B, Bender CM, Erickson KI. Effects of exercise on brain and cognition across age groups and health states. Trends Neurosci. 2020;43(7):533–43. 10.1016/j.tins.2020.04.010. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 39.Beaudart C, Sanchez-Rodriguez D, Locquet M, Reginster JY, Lengelé L, Bruyère O. Malnutrition as a strong predictor of the onset of sarcopenia. Nutrients. 2019;11(12):2883. 10.3390/nu11122883. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 40.Olde Rikkert MG, Verhey FR, Sijben JW, Bouwman FH, Dautzenberg PL, Lansink M, et al. Differences in nutritional status between very mild Alzheimer’s disease patients and healthy controls. J Alzheimer’s Dis. 2014;41:261–71. 10.3233/JAD-13189. [DOI] [PubMed] [Google Scholar]
- 41.Yildiz D, Pekel NB, Kilic AK, Tolgay EN, Tufan F. Malnutrition is associated with dementia severity and geriatric syndromes in patients with Alzheimer disease. Turk J Med Sci. 2015;45(5):1078–81. 10.3906/sag-1406-76. [DOI] [PubMed] [Google Scholar]
- 42.Arıcı H, Tor YB, Altınkaynak M, Erten N, Saka B, Bayramlar OF, et al. Personalized diet with or without physical exercise improves nutritional status, muscle strength, physical performance, and quality of life in malnourished older adults: a prospective randomized controlled study. Nutrients. 2025;17(4):675. 10.3390/nu17040675. [DOI] [PMC free article] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
All data generated or analyzed during this study are available from the corresponding author upon reasonable request.