Table 1.
Summary of theories pertaining to age-related cognitive decline.
Theory/Hypothesis | Reference/s | Summary | General limitations |
---|---|---|---|
The Common-Cause Hypothesis | Baltes and Lindenberger (1997) | • A common biological factor can account for the age-related variance in sensory, sensorimotor and intellectual functioning. | • The focus on one common biological factor neglects much evidence and constructs associated with comprehensive network-based approach to cognitive functioning. |
• Dopaminergic functioning has been proposed as that “common factor” (Li and Lindenberger, 1999). | • Does not consider the role of other monoamines such as noradrenaline and serotonin that modulate neural network activation and neglects other age-related molecular changes. | ||
The Sensory Deprivation Hypothesis | Oster (1976) and Valentijn et al. (2005) | • A lack of adequate sensory input over a prolonged period results in neuronal atrophy, in turn impairing cognitive function. | • Localises cognitive decline to the neural networks dedicated to visual and auditory processing. |
• Neglects a comprehensive neural network-based approach to cognitive functioning. | |||
The Information Degradation Hypothesis | Schneider and Pichora-Fuller (2000) | • Perceptual signals are weakened or degraded due to age-related impairments, resulting in impaired cognitive processing. | • Age-related differences on cognitive tasks are still demonstrated when sensory deficits (in vision and hearing) are corrected (Hall et al., 2005; Anstey et al., 2006). |
• Neglects a comprehensive neural network-based approach to cognitive functioning. | |||
The Processing Speed Theory of Adult Age Differences in Cognition | Salthouse (1996) | • A reduction in the speed at which cognitive operations can be executed, underlies the decline observed in more complex cognitive functions, including memory, problem solving and reasoning. | • Based on findings from paper-pencil measures used with aging populations, without consideration of the confound of motor impairment with age. |
The Inhibitory Deficit Hypothesis | Hasher and Zacks (1988) | • An attention-based model which suggests that good cognitive task performance requires efficient processing of relevant information while simultaneously inhibiting irrelevant information. | • Attention and inhibition of stimuli are highly variable and dependent on the cognitive task (Rey-Mermet and Gade, 2018). |
• Age-group differences in task performance are due to older adults being less efficient in selectively attending to task-relevant stimuli while simultaneously inhibiting task-irrelevant information. | • Tasks used to measure inhibitory control often rely on motor accuracy and response speed on a computerised task, or verbal reaction times, which introduce the potential confound of hand motor speed or slower orofacial movement in an aged population. | ||
The Scaffolding Theory of Aging and Cognition (STAC) | Park and Reuter-Lorenz (2009) | • The STAC integrates evidence from structural and functional neuroimaging to provide a conceptual model of cognitive aging. | • Unclear exactly how compensatory or scaffolding mechanisms are utilized, and how much these compensatory pathways actually contribute to “better” performance. |
• The model proposes that the level of cognitive functioning that an older individual achieves is a consequence of both neural/functional deterioration that requires and utilises compensatory ‘scaffolding’ to attenuate the adverse effects of the neural and functional decline. | • From the viewpoint of STAC, it is unclear how factors that are considered protective against cognitive aging such as higher levels of education or physical activity, strengthen the “scaffolding” mechanism. | ||
The Cognitive Reserve Hypothesis | Stern (2002) | • This hypothesis postulates that individuals who possess a greater ability to recruit and utilise more brain regions, are better able to cope with a greater level of age-related brain pathology before clinical diagnosis is reached. | • Methods of quantifying “cognitive reserve” typically involve inferring reserve from proxy measures such as educational attainment or current occupation. These vary from study to study. |
• It is suggested that this is enabled by means of neural compensation and recruitment of additional brain regions that lead to intact behavioural performance on cognitive tasks. | |||
The Frontal Aging Hypothesis | Jackson (1958) and Dempster (1992) | • This hypothesis is based on the notion that selective frontal lobe pathology in the form of reduced volume, metabolism and simultaneous decline in grey and white matter integrity underlie the cognitive deficits observed in healthy aging. | • Older adults are also impaired in cognitive abilities that are often largely independent of prefrontal areas (Greenwood, 2000). |
• The frontal lobe pathology has predominantly been demonstrated using function magnetic resonance imaging fMRI or PET. | • Whole brain imaging shows that other cortical areas including the temporal and parietal lobes also show compromised integrity with age. | ||
• Neglects a comprehensive neural network-based approach to cognitive functioning. | |||
The Hemispheric Asymmetry Reduction in Older Age (HAROLD) model | Cabeza (2002) | • The HAROLD model is based on the premise that age is related to decreases in lateralisation of brain function, which stem from fMRI observations that young and older adults recruit different neural networks during the same cognitive task (particularly episodic and working memory tasks). | • The HAROLD model has been exclusively described for the PFC, and insight into this model has come from studies using mainly episodic and working memory tasks. |
• It has been reported that young adults display left PFC activation during verbal working memory tasks and right PFC activation during spatial working memory tasks, whereas older adults demonstrate bilateral activation of the PFC while engaging in both verbal and spatial working memory tasks (Reuter-Lorenz et al., 2000). | • Localises cognitive decline to a specific brain region. | ||
• Neglects a comprehensive neural network-based approach to cognitive functioning. | |||
The Compensation-Related Utilization of Neural Circuits Hypothesis (CRUNCH) | Reuter-Lorenz and Cappell (2008) | • The CRUNCH model suggests that declines in neural efficiency across the lifespan results in older adults recruiting more neural resources predominantly in the dorsolateral prefrontal cortex compared to young adults when task demands are low. | • Localises cognitive decline to a particular brain region. |
• However, as task demands increase, neural activation for younger adults exceeds that of older adults, and task performance for older adults is also impaired. | • Neglects a comprehensive neural network-based approach to cognitive functioning. | ||
• When task demands exceed a certain level of difficulty, the aging-brain “falls short” of sufficient activation levels, and task performance declines compared to the younger adults. |