“Lindenberger (2014). Human cognitive aging: Corriger la fortune?” – Article summary

Human cognitive aging differs between individuals. It can be influenced by several factors (e.g. vascular conditions; chronic stress; experience-dependent cognitive plasticity). Living an intellectually challenging, physically active and socially engaged life may mitigate losses to cognition and consolidate gains.

The debilitating effects of old age occur at an increasingly later age. It is possible that the effects of old age reflect limitations in somatic maintenance, resulting in the build up of damage. Factors associated with vascular and metabolic risk (1), inflammation (2), stress (3) and deposition of iron and beta-amyloid (4) accelerate brain aging. However, continued neuroplasticity helps maintain the viability of neural structures and postpone the onset of cognitive decline.

Mechanisms related to maturation and the effects of cold age shape the course of cognitive development from conception to old age. In adulthood and old age, brains show increasing marks of aging but accumulate knowledge and continue to express potential for learning. There are experience-based cognitive abilities called crystallized abilities (e.g. vocabulary) and fluid abilities (e.g. reasoning) which are important in acquiring knowledge. The ages at which cognitive skills reach there peak are likely to reflect a balance among competing processes of knowledge accumulation and deterioration of the supporting neural infrastructure.

Senescence, the effects of old age, affect the neurochemistry and anatomy of the brain (e.g. neurotransmitters show age-related differences in concentration and receptor density). There is a pronounced decrease in dopaminergic neuromodulation. This plays a crucial role in cognitive functioning. Old age is associated with differences in smaller volumes of grey and white matter. Hippocampal shrinkage tends to increase with age and is exacerbated by vascular factors.

White matter hyperintensities (i.e. ischemic lesions; microbleeds; demyelination; expansion of perivascular spaces) tends to increase from middle to late adulthood and is associated with vascular risk and inflammation. The supply-demand mismatch model of adult cognitive plasticity states that the mismatch between functional supply and experienced environmental demands can be caused by primary changes in demand (1) or functional supply (2). Functional supply refers to structural constraints imposed by the brain on function and performance. It permits a given range of performance and functioning. Flexibility refers to the capacity to optimize the brain’s performance within this range. A prolonged mismatch pushes the system away from its current dynamic equilibrium. [CLINICAL DEVELOPMENTAL & HEALTH PSYCHOLOGY, YEAR 3]

The adult brain differs in the onset and degree of age-related volume losses. There are large individual differences in the lateral prefrontal cortex (1), prefrontal white matter (2) and the hippocampus (3). Rates of shrinkage are increased by risk factors (e.g. hypertension; metabolic syndrome; vascular risk). Individual differences in cognitive performance increase from early to late adulthood and old age. It appears as if volume losses in the frontal lobes are interdependent. Deficits in both prefrontal and hippocampal activation patterns contribute interactively to adult age differences in associative episodic memory.

Cognitive aging has a very general component (i.e. there is a general decline rather than a decline on specific tasks). It is not entirely sure what drives age-related cognitive decline. Individuals with lower cognitive abilities are more likely to engage in behaviours that carry risks for late-life cognition (e.g. smoking). Genetic variants may influence age-related differences in cognition. The effects of common genetic polymorphisms on cognition are expected to increase with advancing adult age if the function that relates brain resources to behaviour is assumed to be sigmoid rather than linear. In other words, broad heritability increases from early to late adulthood. However, the observed associations between variations at specific gene loci and individual differences in cognition are small. It is unlikely that individual allelic variations will account for a sizeable portion of phenotypic variance.

Physical exercise improves brain plasticity. The effects are more pronounced for older adults and this may reflect the attenuation of vascular and metabolic risk factors. It is possible that plastic changes are elicited by a mismatch between environmental demand and organismic supply. There is a difference between flexibility and plasticity. Flexibility refers to the capacity for variations in behavioural repertoire that do not require reorganization of brain structure and connections. Plasticity refers to changes in behaviour that do require reorganization of brain structure and connections. Mismatches between supply and demand need to be prolonged to overcome the sluggishness of plasticity and push the system away from its current dynamic equilibrium.

The brains of older adults are less likely to react to environmental challenges with a plastic response because of the metabolic cost (1) and because the older brain has an enormously large behavioural repertoire (2). This means that it is more likely to opt for flexibility rather than plasticity. Down-regulating plasticity during adulthood may favour the emergence of stable social structures. Plasticity appears to decrease from early to late adulthood.

Memory performance is particularly impaired when retrieval depends on self-generated cues and active control processes. When retrieval cues are provided by the environment, age-related deficits in memory tend to disappear. Self-initiated processing and constructive cue generation require maintenance of task representations through recurrent connections between prefrontal and posterior brain regions. The ability to hold representations in mind declines with age. It is likely that cognition starts to rely more on environmental support with age. The greater reliance of older adults on the environment may reflect a long-term adaptation to a cognitive system that is less capable of direction behaviour in a top-down manner.

Attempts at promoting successful aging should, among other things, be directed toward the physical and social environment of the individual. Assistive adaptive technology may foster cognitive maintenance and plasticity by combining support with challenges. This enhances motivation (1), social participation (2) and a sense of autonomy (3) which has positive effects on cognitive development.

There are several different general mechanism linked to favourable aging trajectories:

1. Maintenance
   Brains with well-preserved anatomy and neurochemistry are more likely to generate functional activation patterns that resemble those of younger adults. Therefore, interventions should be aimed at maintaining the state of the brain.
2. Compensation
   High levels of cognitive functioning in old age may reflect instances of successful compensation. Compensation in the context of normal aging refers to structural or functional reorganization of the brain that evolves in response to aging-induced losses in brain functioning. It creates something alternative in response to a loss (e.g. compensatory recruitment of the prefrontal cortex may attenuate the adverse effects of aging on other areas of the brain).
3. Selection
   This refers to being able to execute a given task in multiple ways. Different implementations of a given behaviour may be differentially vulnerable to aging because some brain areas are more resilient than others. Individuals with a larger pool of available processing routes and areas with advancing old age may draw on a greater cognitive reserve that provides a protection against the effects of aging on behaviour.

Beneficial lifestyle choices may attenuate partially modifiable risks (e.g. vascular risks) and it may promote changes that enhance cognition (e.g. neurogenesis).