Skip to main content
Wiley Open Access Collection logoLink to Wiley Open Access Collection
. 2026 Jul 8;88(7):e70190. doi: 10.1002/ajp.70190

A Comparative Study of Aging and Cortical Folding in Chimpanzees and Olive Baboons

William D Hopkins 1,✉, Angela Achorn 1,2, Michele M Mulholland 1, Elizabeth Magden 1, Steven J Schapiro 1, Courtney L Fults 1, Jean‐Francois Mangin 3, Adrien Meguerditchian 4
PMCID: PMC13344867  PMID: 42418262

ABSTRACT

In light of the evidence that nonhuman primates naturally develop Alzheimer's disease neuropathologies, there is a renewed interest in research on the comparative biology of aging, including neurological changes across the age groups in species with diverse lifespans. In this paper, we examined age‐related differences in two measures of cortical folding, mean depth and fold opening, in a sample of chimpanzees (Pan troglodytes) and olive baboons (Papio anubis). We found significant species differences in the slope and pattern of age‐related changes in cortical folding. As predicted, chimpanzees showed negative linear associations between age and mean depth and positive linear associations between age and fold opening, as we see in humans. However, contrary to our hypotheses, baboons showed positive quadratic associations between age and mean depth and negative quadratic associations between age and fold opening. Additionally, within the baboons but not the chimpanzees, significant sex differences were found in age‐related differences in cortical folding. Here, male baboons showed significant linear associations between age, sulci depth, and fold opening, much like male and female chimpanzees. However, for female baboons, slopes of age‐related differences in fold opening were flat or showed slight quadratic associations. It is possible that variation in primate social systems and/or reproductive aging may influence sex and species differences in brain aging. Longitudinal studies on primate brain aging, as well as comparative research with additional taxa, could shed light on the causes and implications of these differences.


This figure shows 3D renderings of a chimpanzee (top) and olive baboon (bottom) brain with each sulcus label used in this study. After sulci were labeled, we exported metrics including mean depth and fold opening (width) of each sulcus to examine age‐related changes in these measures, as well as sex differences within species. We found significant species differences in the slope and pattern of age‐related changes in cortical folding. Additionally, within the baboons but not the chimpanzees, we found significant sex differences in age‐related differences in cortical folding. These findings suggest that variation in social systems and/or reproductive aging may impact sex and species differences in brain aging in nonhuman primates.

graphic file with name AJP-88-e70190-g003.jpg

1. Introduction

A fundamental characteristic of aging in humans is a loss in central nervous system (CNS) integrity. Decades of research have clearly demonstrated that in both healthy and pathological aging, increasing age is associated with a loss in total intracranial, gray and white matter volume, and an increase in the volume of the ventricles (Fjell and Walhovd 2010; Haeger et al. 2020; Liu et al. 2017; Montembeault et al. 2012; Sullivan and Pfefferbaum 2006; Terribilli et al. 2011). Further, the age‐related changes observed in CNS integrity, including in healthy populations, are associated with loss in sensory, motor, and cognitive functions (Bajaj et al. 2018; Bennett and Madden 2014; Coelho et al. 2021; Elliott et al. 2021; Koini et al. 2018; Nazeri et al. 2015; Whalley et al. 2004). Like humans, in nonhuman primates, total intracranial, gray and white matter volume loss has also been reported in multiple primate species in relation to increasing age (Alexander et al. 2008; Autrey et al. 2014; Didier et al. 2016; Frye et al. 2022; Herndon et al. 1999; Koo et al. 2012; Makris et al. 2007; Phillips and Sherwood 2012; Sherwood et al. 2011; Westerhausen et al. 2020; Westerhausen and Meguerditchian 2021; Wisco et al. 2008). Nonhuman primates have also been reported to show decline in motor and cognitive functions with increasing age (Hopkins et al. 2021; Joly et al. 2014; Lacreuse et al. 1999; Lacreuse et al. 2000, 2006, 2014, 2018, 2020; Nagahara et al. 2010; Picq 2007; Herndon et al. 1997; Lai et al. 1995; Moss et al. 1988; Moore et al. 2010; Lacreuse and Herndon 2003; Bachevalier et al. 1991; Frye et al. 2021).

The purpose of this study was to further examine the comparative biology of brain aging in two nonhuman primate species: chimpanzees (Pan troglodytes) and olive baboons (Papio anubis). As in previous studies, we sought to examine age‐related differences in cortical morphology; however, rather than focus on global or region‐specific variation in gray matter or cortical thickness, we assessed aspects of cortical folding, including the mean depth (MD) and sulcal span (or fold opening, FO) of primary and secondary sulci within each species. In humans, recent studies suggest that measuring different dimensions of cortical folding may be more sensitive to age‐related changes than traditional morphological measures such as gray matter volume and cortical thickness (Tang et al. 2021). For example, sulci fold openings (calculated as the ratio of the volume of cerebrospinal fluid in the sulcal basin to surface area of a sulcus) have been shown to be positively associated with age in adult humans (Kochunov et al. 2005) and more sensitive to detecting the onset of brain aging when compared to measures of cortical thickness in the same subjects (Jin et al. 2018; Shu‐Quartier‐Dit‐Maire et al. 2023). Sulci fold opening also differs between patients with probable Alzheimer's disease and controls (Bertoux et al. 2019).

To date, there are few studies on age‐related declines in sulci surface area and depth in nonhuman primates (Kochunov et al. 2010; Hopkins et al. 2023). Kochunov et al. (2010) measured the surface area, length, and sulcal depth of 11 cortical folds using the software program BrainVisa (BV) in 180 baboons. Their subjects included 68 males and 112 females ranging from 7 to 28 years of age (Mean = 16.0 ± 4.2). Depending on the sulcal measure, between three and five sulci were significantly heritable. More germane to this study, linear or quadratic age was a significant covariate for surface area of the cingulate, inferior occipital, occipital‐temporal, principal, and superior temporal folds. For sulci depth, linear or quadratic age was a significant covariate for the cingulate, inferior occipital, lunate, and principal. We note that the direction of the associations is not provided in this paper; thus, though age accounted for a significant proportion of variance in the outcome measures of some sulci, whether they increased or decreased with age was not clear.

Here, like Kochunov et al. (2010), BrainVisa was used to extract the cortical sulci from magnetic resonance image (MRI) scans in a sample of chimpanzees and baboons. From the sulci, the mean depth and fold opening were quantified within each species. Initial analyses examined age differences in each measure for each sulcus within species. Based on patterns observed in humans, we hypothesized that both chimpanzees and baboons would show (1) significant negative associations between age and mean depth and (2) significant positive associations between age and fold opening for one or more sulci. In addition, because sulci are somewhat conserved across different primates, species differences in the slope of age‐related differences in each measure for sulci that are homologous between chimpanzees and baboons were tested in this study. Because chimpanzees and baboons differ in their health, maximum, and median lifespans (Huber et al. 2025), of specific interest were between‐species comparisons in slopes of change for each sulcus and measure. It was hypothesized that the shorter‐lived baboons would show higher slope values across ages compared to the chimpanzees.

2. Methods

2.1. Subjects

Magnetic resonance images (MRI) were obtained from 228 captive chimpanzees housed at the Emory National Primate Research Center (ENPRC, n = 89) in Georgia, USA, and the Center for Chimpanzee Care at The University of Texas M.D. Anderson Cancer Center (UTMDACC, n = 139) in Texas, USA. There were 139 females and 89 males ranging from 6 to 53 years of age in the combined sample (mean = 26.42 years, SD = 10.53). MRI scans were also obtained in 210 baboons (Papio anubis) including 160 females and 50 males ranging between 2.0 and 26.12 years of age (Mean = 10.31 years, SD = 5.75). Eighty‐nine baboons were housed at the Station de Primatologie Centre Nationale Recherche Scientifique in Rousset, France, while the remaining 121 baboons were housed at the UTMDACC. See Table 1 for the full distribution of subjects by age, sex, species, and study site. All subjects were socially housed with continuous full contact in pairs or groups. Subjects had free access to indoor/outdoor enclosures furnished with elevated platforms and vertical climbing structures. Animals received a diet of commercial primate chow, seed/forage, and fresh produce daily and had ad libitum access to water.

Table 1.

Age, sex, and species distribution for subjects included in this study.

Species Study sites Males (n) Females (n) Total (n) Age
Chimpanzee (Pan troglodytes)

UTMDACC: 139

ENPRC: 89

89 139 228

Range = 6–53 years

Mean = 26.42 years

SD = 10.53

Olive baboon (Papio anubis)

UTMDACC: 121

SdP: 89

50 160 210

Range = 2–26 years Mean = 10.31 years

SD = 5.75

Abbreviations: ENPRC = Emory National Primate Research Center (Georgia, USA), SdP = Station de Primatologie Centre Nationale Recherche Scientifique (Rousset, France), UTMDACC = The University of Texas M.D. Anderson Cancer Center (Texas, USA).

2.2. MRI Image Collection

For the chimpanzees, subjects were first immobilized by ketamine (10 mg/kg) or telazol (3–5 mg/kg) and subsequently anaesthetized with propofol (40–60 mg/(kg/h) or isoflurane (1%–3%) following standard procedures at the ENPRC and UTMDACC facilities. ENPRC subjects were then transported to the MRI facility, while UTMDACC subjects were moved to the mobile imaging unit. The subjects remained anaesthetized for the duration of the scans as well as the time needed to transport them between their home enclosures and the imaging facility (between 5 and 10 min) or mobile imaging unit (total time ~5 min). Subjects were placed in the scanner chamber in a supine position with their head fitted inside the head coil. Scan duration ranged between 35 and 55 min as a function of brain size. Seventy‐seven chimpanzees were scanned using a 3.0 Tesla scanner (Siemens Trio, Siemens Medical Solutions USA Inc., Malvern, Pennsylvania, USA) at ENPRC. T1‐weighted images were collected using a three‐dimensional gradient echo sequence (pulse repetition = 2300 ms, echo time = 4.4 ms, number of signals averaged = 3, matrix size = 320 × 320). Additionally, 139 UTMDACC and 12 ENPRC chimpanzees were scanned using a 1.5 Tesla Phillips machine (The Netherlands). T1‐weighted images were collected in the transverse plane using a gradient echo protocol (pulse repetition = 19.0 ms, echo time = 8.5 ms, number of signals averaged = 8, and a 256 × 256 matrix).

For the CNRS baboons, 89 individuals were scanned using a 3.0 Tesla scanner (MEDSPEC 30/80 ADVANCE; Bruker) with a Rapid‐Biomed surface antenna. Subjects were sedated with ketamine (10 mg/kg) before transportation to the Marseille Funcitonal MRI Center. They were then further sedated using tiletamine‐zolazepam (Zoletil; 7 mg/kg) and acepromazine (Calmivet; 0.2–0.5 mg/kg). During the scans, anesthesia was maintained with a drip irrigation of tiletamine‐zolazepam (Zoletil; 4 mg/kg) and NaCI (0.9% of 4 mL/kg/h). The baboons were placed in the scanner chamber in a prone position. High resolution structural T1‐weighted images were acquired (TR: 9.4 ms; TE: 4.3 ms; flip angle: 30°; inversion time: 800 ms); due to size field of view and isotropic voxel size differed for female and young male baboons (fov: 108 × 108 × 108 mm; isotropic voxel size: 0.6 mm3) and adult males (fov: 126 × 126 × 126 mm; isotropic voxel size: 0.7 mm3). Detailed information about both image acquisition and post‐image processing can be found in (Love et al. 2016). For the 121 UTMDACC baboons, images were acquired on a mobile 1.5 Tesla scanner (Phillips Achieva) with either an 8‐channel head coil (young males and all females) or a 6‐channel flex body coil (adult males only). Baboons were sedated using ketamine (10–15 mg/kg), intubated, and maintained on 1%–3% isoflurane anesthesia until the scan was completed. They were placed in the scanner in a supine position, and structural T1‐weighted images were acquired (TR: 17 ms; TE: 3.7 ms; flip angle: 13°; number of signals averaged: 8; matrix size: 133 × 320; voxel resolution: 0.8 mm). After completing MRI procedures, all subjects were temporarily housed in a single enclosure until fully recovered from the anesthesia, after which they were returned to their social group.

2.3. Sulci Extraction and Measurement

The processing used to extract the sulci from the raw T1‐weighted images derives from a pipeline initially dedicated to the human brain and freely distributed as a BrainVISA toolbox (http://brainvisa.info) (Mangin et al. 2004). To account for the differences in chimpanzee and baboon anatomy compared to humans, several adjustments were performed before the scans were processed using the pipeline procedure within BrainVISA. Specifically, chimpanzee and baboon MRI volumes were skull‐stripped and cropped (ANALYZE 12.0), denoised (MRIdenoising for MATLAB; Coupe et al. 2008), N4 bias corrected (3DSlicer), and reformatted at 0.65 mm isotropic resolution (ANALYZE 12.0). These pre‐processed volumes were then imported into BrainVISA. In BrainVisa, the pipeline process of extracting the sulci from the cortex involves multiple steps that have been described in detail for both human and nonhuman primate MRI scans (Mangin et al. 2004). Shown in Figure 1 includes 3D renderings of a chimpanzee and baboon brain showing the cortical sulci labeled in this study within each species (Bailey et al. 1950; Hopkins et al. 2014). There were 9 sulci, including (1) central, (2) arcuate/precentral inferior, (3) rectus/inferior frontal, (4) cingulate, (5) lunate, (6) superior temporal, (7) intraparietal, (8) medial parietal occipital, and (9) sylvian fissure. Measurements of mean depth (MD, in cm) and fold opening (FO, in mm) were obtained for each sulcus from each subject within the two species (see Figure 2).

Figure 1.

Figure 1

3D rendering of a chimpanzee (top) and baboon (bottom) brain with each sulcus label. Chimpanzee sulcus labels include inferior frontal sulcus (IFS), precentral inferior, central sulcus (CS), intraparietal (IP), lunate, superior temporal sulcus (STS), Sylvian fissure (SF), medial parietal occipital (MPO), and cingulate. Baboon sulcus labels include rectus, arcuate, central sulcus (CS), intraparietal (IP), lunate, superior temporal sulcus (STS), and Sylvian fissure (SF).

Figure 2.

Figure 2

Left image: 3D rendering of a human brain with the central sulcus highlighted. Middle image: Once a sulcus is extracted, various measures can be obtained, including length (red line), depth (yellow line), surface area (blue mesh), and sulcal span or fold opening (right image) which reflects the distance between the two sides of the sulcus.

2.4. Data Analysis

Within both the chimpanzee and baboon samples, scans were obtained at two study sites using different magnet strengths. To control for scanner differences, we used Combat Harmonization (Tassi et al. 2024) to adjust MD and FO values for each sulcus while preserving sex and age variables. Our main analyses tested for associations between age and the two outcome measures for each sulcus within the chimpanzee and baboon samples. We performed stepwise multiple regression analyses entering the following variables in order (1) sex, (2) linear age (i.e., age), and (3) curvilinear age (i.e., age2). The inclusion of both linear and curvilinear age allows us to assess linear and quadratic age associations. Changes in the F‐values were tested with the entry of each variable to determine if their inclusion accounted for a significant proportion of variance. The highest order, significant change in F was considered the best fit model.

To test for potential differences in the slope of change for each measure, we averaged the MD and FO scores across all sulci within each species, thereby creating an overall average measure. Because chimpanzees and baboons have different life spans, rather than use their chronological age as the covariate, we computed a centered age value by subtracting the average age for the entire sample from each subject's individual age within each species. Thus, subjects with positive or negative values had ages that were above or below the average for the entire sample within each species. We subsequently performed analysis of covariance on the average z‐scores with species and sex as between‐group factors and centered age as a covariate. For all analyses, the threshold for statistical significance was p < 0.05.

2.5. Research Compliance and Ethics Statement

All animals included in this study were socially housed (continuous full contact—pair or group), and all aspects of this research complied with the American Society of Primatologists' Guidelines for the Ethical use of Non‐Human Primates, NIH policies, and other federal regulations in the United States and France.

3. Results

3.1. Best Fit Model Associations Between Age, Mean Depth, and Fold Opening in Chimpanzees and Baboons

Shown in Tables 2 and 3 are the descriptions of the best‐fit model, r 2 and p values for the associations between age, MD, and FO for each sulcus in the chimpanzees and baboons. We present both the linear and quadratic r 2 values as well as the F‐values associated with the change in R with their inclusion in the statistical model following the variable sex.

Table 2.

R 2 values for linear and quadratic association between age and mean depth.

Linear F‐value r 2 p Quadratic F‐value r 2 p
Baboon
Sylvian fissure 11.70 0.061 0.001 1.33 0.067 0.251
Superior temporal 21.68 0.193 0.001 4.49 0.209 0.035
Cingulate 36.81 0.275 0.001 13.01 0.316 0.001
Lunate 11.94 0.053 0.001 5.43 0.077 0.021
Central 13.90 0.100 0.001 1.11 0.104 0.293
Rectus 51.73 0.205 0.001 11.69 0.246 0.001
Arcuate 30.26 0.167 0.001 14.16 0.218 0.001
Intraparietal 24.63 0.116 0.001 8.58 0.150 0.004
Medial parietal occipital 3.33 0.067 0.069 0.07 0.067 0.786
Average 44.32 0.229 0.001 9.96 0.263 0.002
Chimpanzee
Sylvian fissure 0.18 0.008 0.673 1.71 0.016 0.192
Superior temporal 1.62 0.036 0.204 0.07 0.036 0.791
Cingulate 11.89 0.055 0.001 0.05 0.055 0.819
Lunate 0.03 0.007 0.956 2.20 0.017 0.139
Central 16.49 0.096 0.001 4.40 0.113 0.037
Rectus/inferior frontal 0.84 0.004 0.371 0.87 0.007 0.352
Inferior precentral 2.75 0.017 0.099 0.01 0.017 0.920
Intraparietal 1.04 0.006 0.312 0.46 0.008 0.499
Medial parietal occipital 28.08 0.112 0.001 2.81 0.123 0.095
Average 3.18 0.019 0.076 0.22 0.020 0.639

Table 3.

R 2 values for linear and quadratic association between age and fold opening.

Linear F‐value r 2 p Quadratic F‐value r 2 p
Baboon
Sylvian fissure 45.38 0.186 0.001 5.50 0.207 0.020
Superior temporal 17.49 0.088 0.001 6.92 0.116 0.009
Cingulate 23.22 0.099 0.001 10.04 0.139 0.002
Lunate 5.79 0.070 0.017 11.65 0.118 0.001
Central 15.42 0.080 0.001 6.26 0.107 0.013
Rectus 19.14 0.082 0.000 6.73 0.110 0.010
Arcuate 20.00 0.109 0.000 10.51 0.150 0.001
Intraparietal 9.06 0.091 0.003 6.25 0.117 0.013
Medial parietal occipital 2.99 0.054 0.085 9.19 0.093 0.003
Average 25.72 0.121 0.001 12.45 0.169 0.001
Chimpanzee
Sylvian fissure 2.17 0.013 0.142 1.36 0.019 0.245
Superior temporal 3.27 0.018 0.072 0.81 0.022 0.368
Cingulate 18.02 0.074 0.001 0.26 0.075 0.608
Lunate 0.86 0.001 0.770 4.32 0.020 0.039
Central 11.87 0.050 0.001 0.40 0.050 0.842
Rectus/inferior frontal 9.59 0.051 0.002 1.91 0.059 0.168
Inferior precentral 13.34 0.058 0.001 0.17 0.058 0.684
Intraparietal 2.31 0.012 0.130 1.56 0.019 0.213
Medial parietal occipital 20.77 0.096 0.000 1.23 0.101 0.269
Average 12.23 0.056 0.001 0.44 0.058 0.510

Chimpanzees (Table 2): For the MD (Table 2), significant negative linear correlations were found between age and the cingulate, central, rectus/inferior frontal, and medial parietal occipital sulci, as well as the average of all the sulci. In contrast, and consistent with our hypothesis, for FO (Table 3), age showed significant positive linear associations with the cingulate, central, rectus/inferior frontal, inferior precentral, medial parietal occipital, and the average of all sulci.

Baboons (Table 3): For MD (Table 2), significant negative linear associations were found between age and all 9 sulci as well as their average. Further, significant quadratic associations were found between age and the superior temporal, cingulate, lunate, rectus, arcuate, intraparietal, and the average of all sulci. In these instances, younger and older baboons had higher values compared to middle‐aged individuals. For FO (Table 3), age showed significant linear and quadratic associations with all ninefolds as well as their average. For the quadratic associations, older and younger baboons had lower values than middle‐aged individuals.

3.2. Sex Differences in the Slope in Age Changes Within Chimpanzees and Baboons

Analysis of covariance was used to test whether the slope of change in MD and FO differed between sexes within each species. For each sulcus within the chimpanzee and baboon samples, sex was the between‐group factor while age was the covariate. Sex and age were included as main effect terms as well as their interaction in the statistical models. In the chimpanzees, for both MD and FO, no significant interactions were found between sex and age for any of the sulci; thus, the slope of change across age did not differ between males and females for any measures on any of the sulci. Like for the chimpanzees, for MD, no significant interactions were found between age and sex within the baboon sample. In contrast, the age slopes differed significantly between male and female baboons for multiple sulci for the folding opening measure. For FO, significant two‐way interactions were found between sex and age for the sylvian fissure F(1, 216) = 5.34, p = 0.022, lunate F(1, 214) = 6.38, p = 0.012, central F(1, 214) = 11.53, p = 0.001, arcuate F(1, 216) = 9.39, p = 0.002, medial parietal occipital F(1, 212) = 8.76, p = 0.003, and intraparietal F(1, 214) = 4.97, p = 0.027. Not surprisingly, the interaction between sex and age was also significant for the average of all the folds F(1, 216) = 5.04, p= 0.026. As can be seen in Figure 3, a positive linear association was found between fold opening and age in the males. By contrast, among females, the association between age and fold opening was flat or quadratic, with older and younger individuals having thinner fold opening values.

Figure 3.

Figure 3

Scatterplots of slopes differences in age‐related changes in fold opening between male (blue) and female (red) baboons for six sulci. Fold opening is in millimeters; age is in years.

3.3. Species Differences in the Slope in Age Changes in Sulci Morphology

As reported in Tables 2 and 3, the chimpanzees and baboons appear to exhibit different patterns of association between age and the outcome measures for each sulci. To test whether the slopes statistically differed between species, we performed an additional set of analyses using analysis of covariance comparing the slope in age changes in MD and FO for the average of all the sulci within each species. Species and sex were the between‐group factors, while centered age was the covariate. Because the main result of interest was the interaction(s) between species and centered age, we only report these findings for each sulcus and measure. For MD, a significant two‐way interaction was found between centered age and species MD F(1, 440) = 15.7576, p < 0.001 with baboons showing a greater slope in change compared to the chimpanzees. For FO, a significant three‐way interaction was found between species, sex, and age F(1, 440) = 6.409, p= 0.012 (see Figure 4). Consistent with the results reported in Tables 2 and 3, male and female chimpanzees show linear associations between age, MD, and FO. In contrast, male baboons show linear associations while female baboons show quadratic associations between age, MD, and FO.

Figure 4.

Figure 4

Scatterplots of differences in the best‐fit line between age and the fold opening in baboons (top) and chimpanzees (bottom) for male and female chimpanzees and baboons. Fold opening is in millimeters; age is in years.

4. Discussion

In humans, there is evidence that age‐related sulcal changes correlate with cognitive declines, and it has been suggested that examining these changes could be a tool for diagnosing and monitoring the severity of Alzheimer's disease (AD) (Bertoux et al. 2019). AD is a uniquely human disorder; however, nonhuman primates (NHPs) naturally develop many AD neuropathologies. For example, brains of aged chimpanzees have exhibited amyloid beta protein (Aβ) in plaques and blood vessels, pretangles, neurofibrillary tangles (NFT), and tau immunoreactive neuritic clusters (Edler et al. 2017). Research on the comparative biology of brain aging in NHPs, including age‐related sulcal alterations, can therefore contribute to our understanding of AD pathogenesis and progression in humans. Additionally, these findings can also inform evolutionary perspectives on aging in the primate order.

In this study, we examined age‐related differences in cortical folding in chimpanzees and olive baboons. The main finding is that chimpanzees and baboons showed different patterns of cross‐sectional associations between age, mean depth, and fold opening across multiple sulci. Specifically, older chimpanzees had lower mean depths and larger sulcal spans. Broadly speaking, the findings from the chimpanzees are similar to reports in humans (Jin et al. 2018). In contrast, the pattern of age‐related differences in sulcal morphology in baboons differ from chimpanzees and from reports from humans across measures. For mean depth, contrary to our hypothesis, older and younger baboons had higher depth values than middle‐aged individuals for most of the sulci. Similarly, we predominantly found significant quadratic associations between age and fold opening, with older and younger baboons having lower values. The differences in cross‐sectional age changes in sulci morphology were particularly evident when comparing chimpanzees and baboons on the average of all sulci labeled within each species (see Figure 4).

The explanation for species differences in the pattern of aging in cortical folding is not clear, but arguably the most parsimonious is that the longer life span of chimpanzees results in increased risk for the onset of neurodegeneration at different morphological levels of analysis, which manifests as more robust associations between age and each outcome measure compared to the baboons. The limitation of this interpretation is that it does not explain species differences in the pattern of association per se. That is, this does not explain why the baboons show largely quadratic associations between age, mean depth, and fold opening whereas the chimpanzees show linear associations. Indeed, in light of the differences in lifespan and health‐span between chimpanzees and baboons, we expected that (1) both species would exhibit inverse linear associations between age and mean depth and positive associations with fold opening, and (2) the slope of change would be greater in the more short‐lived baboons compared to the chimpanzees. The hypothesized patterns of age‐related differences in cortical folding for MD and FO are largely supported in the chimpanzees but less consistent or absent in the baboons. It is also possible that the age ranges, as a proportion of lifespan, were not fully equivalent between the two species which could impact the slope of change across ages. In other words, a disproportionally lower or higher number of young or elderly subjects in one species could impact the slope across age. We cannot rule out this possibility, but based on the median health‐span age for each species as reported by Huber et al. (2025), the age ranges appear comparable.

The quadratic associations between age, MD, and FO in the baboons may also be explained by the cross‐sectional nature of this study, particularly for the oldest animals. Within the context of lifespan, the oldest baboons in this study are those that have lived the longest and in human parlance might be considered “super agers”, that being, individuals who live exceptionally long without exhibiting significant cognitive and neurological impairment (de Godoy et al. 2021). In the case of older baboons, these individuals may have specific neuroprotective processes that have slowed their aging process compared to the similarly aged baboons that are deceased and therefore not represented in the sample of baboons on which MRI scans were obtained in this study. This possibility highlights the significant need for longitudinal rather than cross‐sectional studies on age‐related changes in brain and cognition in nonhuman primates.

Within the baboons, significant sex differences were found with males showing significant linear associations between age and fold opening, whereas either significant quadratic or no associations were found in females. In contrast, we found no evidence of significant differences in the slope of change for MD or FO between male and female chimpanzees. Why male and female baboons show different patterns of age‐related differences in fold opening is not clear; however, it is worth noting that baboon social structure differs from that of chimpanzees. Though both species live in multi‐male, multi‐female societies, the baboon social organization is matrifocal compared to the patrifocal organization found in chimpanzees. Some have suggested that higher‐ranking males within the matrifocal social system of baboons (who also tend to be older) experience greater allostatic load across the life span, which results in accelerated aging, possibly via epigenetic processes (Anderson et al. 2021; Tung et al. 2016). That said, a previous study in baboons at the UTMDACC failed to find sex differences in epigenetic aging (Neal et al. 2025). Alternatively, the observed sex differences in fold opening in baboons but not chimpanzees could relate to reproductive aging. That is, female chimpanzees typically experience a longer post‐menopausal lifespan than female baboons. In humans, research has shown that menopause can influence both brain structure and cognitive aging (e.g., Ramli et al. 2023). Additional research examining whether differences in reproductive aging influence patterns of brain aging across primate species could shed light on the potential mechanisms underlying our findings.

One limitation of this study, and indeed all studies of brain aging in nonhuman primates, is the cross‐sectional design. Like in humans, cross‐sectional studies in nonhuman primates are also subject to cohort effects, and the findings reported here are no exception. For example, some have hypothesized that captive rearing practices, diet, animal welfare, and enrichment programs have changed in the past 30 years, and these changes may impact age‐related differences in brain and cognitive functions (Walker and Jucker 2017). Thus, baboons or chimpanzees born in captivity 20–30 years ago likely experienced different rearing, behavioral, and cognitive enrichment experiences compared to individuals, for example, born 5–10 years ago. This limitation speaks directly to the need for longitudinal studies on age‐related changes in the brain and cognition in nonhuman primates. Additionally, for the chimpanzees, we did not make fine distinctions nor account for minor variations in the sulci patterns that have been employed in previous studies (Amiez et al. 2019; Falk et al. 2018; Hopkins et al. 2022; Miller et al. 2020, 2021). For example, the inferior frontal sulcus fuses with the rectus in ~50% of chimpanzee brains (Hopkins et al. 2022). Here, we did not apply this distinction between the rectus and inferior frontal sulcus and, instead, labeled them as a single sulcus.

5. Conclusion

In summary, the findings presented here suggest that chimpanzees and baboons show dissimilar patterns of age‐related differences in cortical folding. Sex differences in age‐related changes in cortical folding were evident in baboons but not chimpanzees. Indeed, male baboons showed predictable and significant linear associations between age, sulci depth, and fold opening, much like male and female chimpanzees. By contrast, slopes of age‐related differences in fold opening in female baboons were flat or, if anything, showed a quadratic association. These collective results suggest the possibility that differences in primate social structure and/or reproductive aging may mediate sex‐dependent changes in brain structure across the lifespan. Longitudinal studies on primate brain aging, as well as comparative research with additional taxa, would be especially valuable for evaluating this hypothesis and understanding potential implications of these differences.

Author Contributions

William D. Hopkins: conceptualization, investigation, funding acquisition, writing – original draft, methodology, formal analysis, project administration, resources, writing – review and editing. Angela Achorn: writing – review and editing, formal analysis, investigation, writing – original draft. Michele M. Mulholland: investigation, writing – original draft, funding acquisition, resources. Elizabeth Magden: resources. Steven J. Schapiro: resources. Courtney L. Fults: formal analysis. Jean‐Francois Mangin: writing – review and editing, resources. Adrien Meguerditchian: writing – review and editing, resources.

Acknowledgments

This work was supported, in part, by NSF grant 2021711 and NIH grants AG‐067419, AG‐078411, AG‐087914, OD‐024628, and NS‐092988. A.M. has received funding from the European Research Council under the European Union's Horizon 2020 research and innovation program grant agreement No 716931— GESTIMAGE—ERC‐2016‐STG, from the French “Agence Nationale de le Recherche” ANR‐12‐PDOC‐0014‐01 (LangPrimate), ANR‐23‐CE28‐0029‐01 (BABONTO), ANR‐16‐CONV‐0002 (ILCB), and from the Excellence Initiative of Aix Marseille University (A*MIDEX). MRI acquisitions were done at the Center IRM‐INT (UMR 7289, AMU CNRS), platform member of France Life Imaging network (grant ANR‐11‐INBS‐0006). Chimpanzee maintenance at the National Center for Chimpanzee Care was previously funded by NIH/NCRR U42—OD—011197. All animals included in this study were socially housed, and all aspects of this research complied with the American Society of Primatologists' Guidelines for the Ethical use of non‐human primates, NIH policies, and other federal regulations in the United States and France. Reprint requests may be sent to: William D. Hopkins, Department of Comparative Medicine, Keeling Center for Comparative Medicine and Research, Bastrop, Texas 78602. Email: wdhopkins@mdanderson.org .

References

  1. Alexander, G. E. , Chen K., Aschenbrenner M., et al. 2008. “Age‐Related Regional Network of Magnetic Resonance Imaging Gray Matter in the Rhesus Macaque.” Journal of Neuroscience 28, no. 11: 2710–2718. 10.1523/jneurosci.1852-07.2008. [DOI] [PMC free article] [PubMed] [Google Scholar]
  2. Amiez, C. , Sallet J., Hopkins W. D., et al. 2019. “Sulcal Organization in the Medial Frontal Cortex Provides Insights into Primate Brain Evolution.” Nature Communications 10: 3437. [DOI] [PMC free article] [PubMed] [Google Scholar]
  3. Anderson, J. A. , Johnston R. A., Lea A. J., et al. 2021. “High Social Status Males Experience Accelerated Epigenetic Aging in Wild Baboons.” eLife 10. 10.7554/eLife.66128. [DOI] [PMC free article] [PubMed] [Google Scholar]
  4. Autrey, M. M. , Reamer L. A., Mareno M. C., et al. 2014. “Age‐Related Effects in the Neocortical Organization of Chimpanzees: Gray and White Matter Volume, Cortical Thickness, and Gyrification.” NeuroImage 101: 59–67. 10.1016/j.neuroimage.2014.06.053. [DOI] [PMC free article] [PubMed] [Google Scholar]
  5. Bachevalier, J. , Landis L. S., Walker L. C., et al. 1991. “Aged Monkeys Exhibit Behavioral Deficits Indicative of Widespread Cerebral Dysfunction.” Neurobiology of Aging 12, no. 2: 99–111. 10.1016/0197-4580(91)90048-o. [DOI] [PubMed] [Google Scholar]
  6. Bailey, P. , von Bonin G., and McCulloch W. S.. 1950. The Isocortex of the Chimpanzee. University of Illinois Press. [Google Scholar]
  7. Bajaj, S. , Raikes A., Smith R., et al. 2018. “The Relationship Between General Intelligence and Cortical Structure in Healthy Individuals.” Neuroscience 388: 36–44. 10.1016/j.neuroscience.2018.07.008. [DOI] [PubMed] [Google Scholar]
  8. Bennett, I. J. , and Madden D. J.. 2014. “Disconnected Aging: Cerebral White Matter Integrity and Age‐Related Differences in Cognition.” Neuroscience 276: 187–205. 10.1016/j.neuroscience.2013.11.026. [DOI] [PMC free article] [PubMed] [Google Scholar]
  9. Bertoux, M. , Lagarde J., Corlier F., et al. 2019. “Sulcal Morphology in Alzheimer's Disease: An Effective Marker of Diagnosis and Cognition.” Neurobiology of Aging 84: 41–49. 10.1016/j.neurobiolaging.2019.07.015. [DOI] [PubMed] [Google Scholar]
  10. Coelho, A. , Fernandes H. M., Magalhães R., et al. 2021. “Signatures of White‐Matter Microstructure Degradation During Aging and Its Association With Cognitive Status.” Scientific Reports 11, no. 1: 4517. 10.1038/s41598-021-83983-7. [DOI] [PMC free article] [PubMed] [Google Scholar]
  11. Coupe, P. , Yger P., Prima S., Hellier P., Kervrann C., and Barillot C.. 2008. “An Optimized Blockwise Nonlocal Means Denoising Filter for 3‐D Magnetic Resonance Images.” IEEE Transactions on Medical Imaging 27, no. 4: 425–441. 10.1109/TMI.2007.906087. [DOI] [PMC free article] [PubMed] [Google Scholar]
  12. de Godoy, L. L. , Alves C. A. P. F., Saavedra J. S. M., et al. 2021. “Understanding Brain Resilience in Superagers: A Systematic Review.” Neuroradiology 63, no. 5: 663–683. 10.1007/s00234-020-02562-1. [DOI] [PubMed] [Google Scholar]
  13. Didier, E. S. , MacLean A. G., Mohan M., Didier P. J., Lackner A. A., and Kuroda M. J.. 2016. “Contributions of Nonhuman Primates to Research on Aging.” Veterinary Pathology 53, no. 2: 277–290. 10.1177/0300985815622974. [DOI] [PMC free article] [PubMed] [Google Scholar]
  14. Edler, M. K. , Sherwood C. C., Meindl R. S., et al. 2017. “Aged Chimpanzees Exhibit Pathologic Hallmarks of Alzheimer's Disease.” Neurobiology of Aging 59: 107–120. 10.1016/j.neurobiolaging.2017.07.006. [DOI] [PMC free article] [PubMed] [Google Scholar]
  15. Elliott, M. L. , Belsky D. W., Knodt A. R., et al. 2021. “Brain‐Age in Midlife Is Associated With Accelerated Biological Aging and Cognitive Decline in a Longitudinal Birth Cohort.” Molecular Psychiatry 26, no. 8: 3829–3838. 10.1038/s41380-019-0626-7. [DOI] [PMC free article] [PubMed] [Google Scholar]
  16. Falk, D. , Zollikofer C. P. E., Ponce de León M., Semendeferi K., Alatorre Warren J. L., and Hopkins W. D.. 2018. “Identification of In Vivo Sulci on the External Surface of Eight Adult Chimpanzee Brains: Implications for Interpreting Early Hominin Endocasts.” Brain Behavior and Evolution 91, no. 1: 45–58. 10.1159/000487248. [DOI] [PubMed] [Google Scholar]
  17. Fjell, A. M. , and Walhovd K. B.. 2010. “Structural Brain Changes in Aging: Courses, Causes and Cognitive Consequences.” Reviews in the Neurosciences 21, no. 3: 187–221. 10.1515/revneuro.2010.21.3.187. [DOI] [PubMed] [Google Scholar]
  18. Frye, B. M. , Craft S., Register T. C., et al. 2022. “Early Alzheimer's Disease‐Like Reductions in Gray Matter and Cognitive Function With Aging in Nonhuman Primates.” Alzheimer's & Dementia 8, no. 1: e12284. 10.1002/trc2.12284. [DOI] [PMC free article] [PubMed] [Google Scholar]
  19. Frye, B. M. , Valure P. M., Craft S., et al. 2021. “Temporal Emergence of Age‐Associated Changes in Cognitive and Physical Function in Vervets (Chlorocebus aethiops sabaeus).” GeroScience 43, no. 3: 1303–1315. 10.1007/s11357-021-00338-w. [DOI] [PMC free article] [PubMed] [Google Scholar]
  20. Haeger, A. , Mangin J. F., Vignaud A., et al. 2020. “Imaging the Aging Brain: Study Design and Baseline Findings of the SENIOR Cohort.” Alzheimer's Research & Therapy 12, no. 1: 77. 10.1186/s13195-020-00642-1. [DOI] [PMC free article] [PubMed] [Google Scholar]
  21. Herndon, J. G. , Moss M. B., Rosene D. L., and Killiany R. J.. 1997. “Patterns of Cognitive Decline in Aged Rhesus Monkeys.” Behavioural Brain Research 87: 25–34. [DOI] [PubMed] [Google Scholar]
  22. Herndon, J. G. , Tigges J., Anderson D. C., Klumpp S. A., and McClure H. M.. 1999. “Brain Weight Throughout the Life Span of the Chimpanzee.” Journal of Comparative Neurology 409: 567–572. [PubMed] [Google Scholar]
  23. Hopkins, W. D. , Coulon O., Meguerditchian A., et al. 2023. “Genetic Determinants of Individual Variation in the Superior Temporal Sulcus of Chimpanzees (Pan troglodytes).” Cerebral Cortex 33: 1925–1940. 10.1093/cercor/bhac183. [DOI] [PMC free article] [PubMed] [Google Scholar]
  24. Hopkins, W. D. , Mareno M. C., Neal Webb S. J., Schapiro S. J., Raghanti M. A., and Sherwood C. C.. 2021. “Age‐Related Changes in Chimpanzee (Pan troglodytes) Cognition: Cross‐Sectional and Longitudinal Analyses.” American Journal of Primatology 83, no. 3: e23214. 10.1002/ajp.23214. [DOI] [PMC free article] [PubMed] [Google Scholar]
  25. Hopkins, W. D. , Meguerditchian A., Coulon O., et al. 2014. “Evolution of the Central Sulcus Morphology in Primates.” Brain, Behavior and Evolution 84: 19–30. [DOI] [PMC free article] [PubMed] [Google Scholar]
  26. Hopkins, W. D. , Sprung‐Much T., Amiez C., et al. 2022. “A Comprehensive Analysis of Variability in the Sulci That Define the Inferior Frontal Gyrus in the Chimpanzee (Pan troglodytes) Brain.” American Journal of Biological Anthropology 179, no. 1: 31–47. [Google Scholar]
  27. Huber, H. F. , Ainsworth H. C., Quillen E. E., et al. 2025. “Comparative Lifespan and Healthspan of Nonhuman Primate Species Common to Biomedical Research.” GeroScience 47, no. 1: 135–151. 10.1007/s11357-024-01421-8. [DOI] [PMC free article] [PubMed] [Google Scholar]
  28. Jin, K. , Zhang T., Shaw M., Sachdev P., and Cherbuin N.. 2018. “Relationship Between Sulcal Characteristics and Brain Aging.” Frontiers in Aging Neuroscience 10: 339. 10.3389/fnagi.2018.00339. [DOI] [PMC free article] [PubMed] [Google Scholar]
  29. Joly, M. , Ammersdörfer S., Schmidtke D., and Zimmermann E.. 2014. “Touchscreen‐Based Cognitive Tasks Reveal Age‐Related Impairment in a Primate Aging Model, the Grey Mouse Lemur (Microcebus murinus).” PLoS One 9, no. 10: e109393. 10.1371/journal.pone.0109393. [DOI] [PMC free article] [PubMed] [Google Scholar]
  30. Kochunov, P. , Glahn D. C., Fox P. T., et al. 2010. “Genetics of Primary Cerebral Gyrification: Heritability of Length, Depth and Area of Primary Sulci in an Extended Pedigree of Papio Baboons.” NeuroImage 53, no. 3: 1126–1134. [DOI] [PMC free article] [PubMed] [Google Scholar]
  31. Kochunov, P. , Mangin J. F., Coyle T., et al. 2005. “Age‐Related Morphology Trends of Cortical Sulci.” Human Brain Mapping 26, no. 3: 210–220. [DOI] [PMC free article] [PubMed] [Google Scholar]
  32. Koini, M. , Duering M., Gesierich B. G., et al. 2018. “Grey‐Matter Network Disintegration as Predictor of Cognitive and Motor Function With Aging.” Brain Structure and Function 223, no. 5: 2475–2487. 10.1007/s00429-018-1642-0. [DOI] [PMC free article] [PubMed] [Google Scholar]
  33. Koo, B. B. , Schettler S. P., Murray D. E., et al. 2012. “Age‐Related Effects on Cortical Thickness Patterns of the Rhesus Monkey Brain.” Neurobiology of Aging 33: 200.e23–200.e31. [DOI] [PMC free article] [PubMed] [Google Scholar]
  34. Lacreuse, A. , Espinosa P. M., and Herndon J. G.. 2006. “Relationships Among Cognitive Function, Fine Motor Speed and Age in the Rhesus Monkey.” Age 28, no. 3: 255–264. 10.1007/s11357-006-9019-3. [DOI] [PMC free article] [PubMed] [Google Scholar]
  35. Lacreuse, A. , and Herndon J. G.. 2003. “Effects of Estradiol and Aging on Fine Manual Performance in Female Rhesus Monkeys.” Hormones and Behavior 43, no. 3: 359–366. https://www.ncbi.nlm.nih.gov/pubmed/12695108. [DOI] [PubMed] [Google Scholar]
  36. Lacreuse, A. , Herndon J. G., Killiany R. J., Rosene D. L., and Moss M. B.. 1999. “Spatial Cognition in Rhesus Monkeys: Male Superiority Declines With Age.” Hormones and Behavior 36, no. 1: 70–76. 10.1006/hbeh.1999.1532. [DOI] [PubMed] [Google Scholar]
  37. Lacreuse, A. , Herndon J. G., and Moss M. B.. 2000. “Cognitive Function in Aged Ovariectomized Female Rhesus Monkeys.” Behavioral Neuroscience 114, no. 3: 506–513. https://www.ncbi.nlm.nih.gov/pubmed/10883801. [DOI] [PubMed] [Google Scholar]
  38. Lacreuse, A. , Parr L., Chennareddi L., and Herndon J. G.. 2018. “Age‐Related Decline in Cognitive Flexibility in Female Chimpanzees.” Neurobiology of Aging 72: 83–88. 10.1016/j.neurobiolaging.2018.08.018. [DOI] [PMC free article] [PubMed] [Google Scholar]
  39. Lacreuse, A. , Raz N., Schmidtke D., Hopkins W. D., and Herndon J. G.. 2020. “Age‐Related Decline in Executive Function as a Hallmark of Cognitive Ageing in Primates: An Overview of Cognitive and Neurobiological Studies.” Philosophical Transactions of the Royal Society, B: Biological Sciences 375, no. 1811: 20190618. 10.1098/rstb.2019.0618. [DOI] [PMC free article] [PubMed] [Google Scholar]
  40. Lacreuse, A. , Russell J. L., Hopkins W. D., and Herndon J. G.. 2014. “Cognitive and Motor Aging in Female Chimpanzees.” Neurobiology of Aging 35, no. 3: 623–632. [DOI] [PMC free article] [PubMed] [Google Scholar]
  41. Lai, Z. C. , Moss M. B., Killiany R. J., Rosene D. L., and Herndon J. G.. 1995. “Executive System Dysfunction in the Aged Monkey: Spatial and Object Reversal Learning.” Neurobiology of Aging 16, no. 6: 947–954. 10.1016/0197-4580(95)02014-4. [DOI] [PubMed] [Google Scholar]
  42. Liu, K. , Yao S., Chen K., et al. 2017. “Structural Brain Network Changes Across the Adult Lifespan.” Frontiers in Aging Neuroscience 9: 275. 10.3389/fnagi.2017.00275. [DOI] [PMC free article] [PubMed] [Google Scholar]
  43. Love, S. A. , Marie D., Roth M., et al. 2016. “The Average Baboon Brain: MRI Templates and Tissue Probability Maps From 89 Individuals.” NeuroImage 132: 526–533. 10.1016/j.neuroimage.2016.03.018. [DOI] [PubMed] [Google Scholar]
  44. Makris, N. , Papadimitriou G. M., van der Kouwe A., et al. 2007. “Frontal Connections and Cognitive Changes in Normal Aging Rhesus Monkeys: A DTI Study.” Neurobiology of Aging 28, no. 10: 1556–1567. 10.1016/j.neurobiolaging.2006.07.005. [DOI] [PubMed] [Google Scholar]
  45. Mangin, J. F. , Riviere D., Cachia A., et al. 2004. “Object‐Based Morphometry of the Cerebral Cortex.” IEEE Transactions on Medical Imaging 23, no. 8: 968–982. [DOI] [PubMed] [Google Scholar]
  46. Miller, E. N. , Hof P. R., Sherwood C. C., and Hopkins W. D.. 2021. “The Paracingulate Sulcus Is a Unique Feature of the Medial Frontal Cortex Shared by Great Apes and Humans.” Brain, Behavior and Evolution 96, no. 1: 26–36. 10.1159/000517293. [DOI] [PubMed] [Google Scholar]
  47. Miller, J. A. , Voorhies W. I., Li X., et al. 2020. “Sulcal Morphology of Ventral Temporal Cortex Is Shared Between Humans and Other Hominoids.” Scientific Reports 10, no. 1: 17132. 10.1038/s41598-020-73213-x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  48. Montembeault, M. , Joubert S., Doyon J., et al. 2012. “The Impact of Aging on Gray Matter Structural Covariance Networks.” NeuroImage 63, no. 2: 754–759. 10.1016/j.neuroimage.2012.06.052. [DOI] [PubMed] [Google Scholar]
  49. Moore, T. L. , Killiany R. J., Pessina M. A., Moss M. B., and Rosene D. L.. 2010. “Assessment of Motor Function of the Hand in Aged Rhesus Monkeys.” Somatosensory & Motor Research 27, no. 3: 121–130. 10.3109/08990220.2010.485963. [DOI] [PMC free article] [PubMed] [Google Scholar]
  50. Moss, M. B. , Rosene D. L., and Peters A.. 1988. “Effects of Aging on Visual Recognition Memory in the Rhesus Monkey.” Neurobiology of Aging 9: 495–502. [DOI] [PubMed] [Google Scholar]
  51. Nagahara, A. H. , Bernot T., and Tuszynski M. H.. 2010. “Age‐Related Cognitive Deficits in Rhesus Monkeys Mirror Human Deficits on an Automated Test Battery.” Neurobiology of Aging 31, no. 6: 1020–1031. [DOI] [PMC free article] [PubMed] [Google Scholar]
  52. Nazeri, A. , Chakravarty M. M., Rajji T. K., et al. 2015. “Superficial White Matter as a Novel Substrate of Age‐Related Cognitive Decline.” Neurobiology of Aging 36, no. 6: 2094–2106. 10.1016/j.neurobiolaging.2015.02.022. [DOI] [PubMed] [Google Scholar]
  53. Neal, S. J. , Whitney S., Yi S. V., and Simmons J. H.. 2025. “Epigenetic and Accelerated Age in Captive Olive Baboons (Papio anubis), and Relationships With Walking Speed and Fine Motor Performance.” Aging 17, no. 3: 740–756. [DOI] [PMC free article] [PubMed] [Google Scholar]
  54. Phillips, K. A. , and Sherwood C. C.. 2012. “Age‐Related Differences in Corpus Callosum Area of Capuchin Monkeys.” Neuroscience 202: 202–208. 10.1016/j.neuroscience.2011.11.074. [DOI] [PMC free article] [PubMed] [Google Scholar]
  55. Picq, J. 2007. “Aging Affects Executive Functions and Memory in Mouse Lemur Primates.” Experimental Gerontology 42, no. 3: 223–232. 10.1016/j.exger.2006.09.013. [DOI] [PubMed] [Google Scholar]
  56. Ramli, N. Z. , Yahaya M. F., Mohd Fahami N. A., Abdul Manan H., Singh M., and Damanhuri H. A.. 2023. “Brain Volumetric Changes in Menopausal Women and Its Association With Cognitive Function: A Structured Review.” Frontiers in Aging Neuroscience 25, no. 15: 1158001. 10.3389/fnagi.2023.1158001. [DOI] [PMC free article] [PubMed] [Google Scholar]
  57. Sherwood, C. C. , Gordon A. D., Allen J. S., et al. 2011. “Aging of the Cerebral Cortex Differs Between Humans and Chimpanzees.” Proceedings of the National Academy of Sciences 108: 13029–13034. [DOI] [PMC free article] [PubMed] [Google Scholar]
  58. Shu‐Quartier‐Dit‐Maire, W. , Le Guen Y., Bouteloup V., Frouin V., Dufouil C., and Mangin J. F.. 2023. Considering Sulcal Width Rather Than Cortical Thickness to Assess Brain Atrophy in Ageing. The Organization for Human Brain Mapping, Montreal, Canada. [Google Scholar]
  59. Sullivan, E. V. , and Pfefferbaum A.. 2006. “Diffusion Tensor Imaging and Aging.” Neuroscience & Biobehavioral Reviews 30, no. 6: 749–761. 10.1016/j.neubiorev.2006.06.002. [DOI] [PubMed] [Google Scholar]
  60. Tang, H. , Liu T., Liu H., et al. 2021. “A Slower Rate of Sulcal Widening in the Brains of the Nondemented Oldest Old.” NeuroImage 229: 117740. 10.1016/j.neuroimage.2021.117740. [DOI] [PubMed] [Google Scholar]
  61. Tassi, E. , Bianchi A. M., Calesella F., et al. 2024. “Assessment of Combat Harmonization Performance on Structural Magnetic Resonance Imaging Measurements.” Human Brain Mapping 45, no. 18: e70085. 10.1002/hbm.70085. [DOI] [PMC free article] [PubMed] [Google Scholar]
  62. Terribilli, D. , Schaufelberger M. S., Duran F. L. S., et al. 2011. “Age‐Related Gray Matter Volume Changes in the Brain During Non‐Elderly Adulthood.” Neurobiology of Aging 32, no. 2: 354–368. 10.1016/j.neurobiolaging.2009.02.008. [DOI] [PMC free article] [PubMed] [Google Scholar]
  63. Tung, J. , Archie E. A., Altmann J., and Alberts S. C.. 2016. “Cumulative Early Life Adversity Predicts Longevity in Wild Baboons.” Nature Communications 7: 11181. 10.1038/ncomms11181. [DOI] [PMC free article] [PubMed] [Google Scholar]
  64. Walker, L. C. , and Jucker M.. 2017. “The Exceptional Vulnerability of Humans to Alzheimer's Disease.” Trends in Molecular Medicine 23, no. 6: 534–545. 10.1016/j.molmed.2017.04.001. [DOI] [PMC free article] [PubMed] [Google Scholar]
  65. Westerhausen, R. , Fjell A. M., Kompus K., et al. 2021. “Comparative Morphology of the Corpus Callosum Across the Adult Lifespan in Chimpanzees (Pan troglodytes) and Humans.” Journal of Comparative Neurology 529: 1584–1596. 10.1002/cne.25039. [DOI] [PMC free article] [PubMed] [Google Scholar]
  66. Westerhausen, R. , and Meguerditchian A.. 2021. “Corpus Callosum Morphology Across the Lifespan in Baboons (Papio anubis): A Cross‐Sectional Study of Relative Mid‐Sagittal Surface Area and Thickness.” Neuroscience Research 171: 19–26. 10.1016/j.neures.2021.03.002. [DOI] [PubMed] [Google Scholar]
  67. Whalley, L. J. , Deary I. J., Appleton C. L., and Starr J. M.. 2004. “Cognitive Reserve and the Neurobiology of Cognitive Aging.” Ageing Research Reviews 3: 369–382. [DOI] [PubMed] [Google Scholar]
  68. Wisco, J. J. , Killiany R. J., Guttmann C. R. G., Warfield S. K., Moss M. B., and Rosene D. L.. 2008. “An MRI Study of Age‐Related White and Gray Matter Volume Changes in the Rhesus Monkey.” Neurobiology of Aging 29, no. 10: 1563–1575. 10.1016/j.neurobiolaging.2007.03.022. [DOI] [PMC free article] [PubMed] [Google Scholar]

Articles from American Journal of Primatology are provided here courtesy of Wiley

RESOURCES