Article 7: Human cognitive aging: Corriger la fortune? (Lindenberger)

Question 1

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Answer 1

• the debilitating effects of senescence are not being stretched out in time but delayed to later ages
• onset of cognitive decline later than suggested by cross-sectional studiescohort effects
• Adult cognitive development individual
• the shape and course of adult cognitive development is best conceived as a range of potential developmental trajectories that reflect person-specific endowments and environmental opportunities and constraints
• range of potentially available developmental trajectories is likely to differ from person to person
• neuroplasticity
• epigenetics

Fluid and crystallized cognitive abilities
• the ages at which cognitive skills reach their peak are likely to reflect a balance among competing processes of knowledge accumulation and deterioration of the supporting neural infrastructure
The senescent brain
• Many neurotransmitters show marked age-related differences in concentration and receptor density
• Dopaminergic neuromodulation: pronounced age-related decrease in dopaminergic neuromodulation in healthy older adults.
• dopamine plays a critical role in cognitive functioning
• reduced size and weight, expansion of cerebral ventricles and sulci, deformation and loss of myelin sheathing, region-specific loss of dendritic arborization and neuronal bodies, rarefication of cerebral vasculature, and reduced synaptic density
• smaller volumes of gray and white matter.
• Polymodal cortical regions display greater volume reductions than other neocortical areas, whereas primary visual cortices show relatively little volume loss
• Hippocampus shrinking (?)
• White matter hyperintensities, which reflect ischemic lesions, microbleeds, demyelination, and expansion of perivascular spaces, increase from middle to late adulthood and show associations with vascular risk and genetic variants related to inflammation
• decreasing white matter integrity with advancing adult age
• primates: the degeneration of thin synaptic spines in dorsolateral prefrontal cortex, as well as synaptic alterations in the dentate gyrus of the hippocampus, contribute to age related losses in memory
• Rodent models indicate that normal aging alters excitatory synaptic transmission in hippocampal granule cells and in CA3 and CA1 pyramidal cells

Individual differences in change
• .Lateral prefrontal cortex, prefrontal white matter, and the hippocampus are among the regions that show particularly large individual differences in age-related shrinkage
• Differences increase with age, environmental and genetic
• One study found that shrinkage of prefrontal white matter correlated with shrinkage of lateral prefrontal cortex(r=0.71) and with shrinkage of hippocampal volumes(r= 0.70),indicating that volume losses in the frontal lobes and in medial-temporal cortex are interdependent
• Ageing: strong general component
• decrements in dopamine availability in striatal and cortical brain regions (21–23); anatomical changes in medial-temporal(46)and prefrontal(47) areas; structural and functional connectivity decrements due to white matter alteration ;a compromised dynamic range of neural activation (50); and deficient synchronization of oscillatory activity within and across fast and slow frequencies
• effects of genetic polymorphisms increase with age
• neurotrophic factor (BDNF) gene (62), the dopamine D2 receptor and transporter genes (63), and the dopamine and glutamate receptor geneseffects on episodic memory
• D2 and D3 receptor genes and the DA transporter gene forgetting rates
• dopamine D2 receptor genes response inhibition
• broad heritability increases from early to late adulthood
• unlikely that individual allelic variations will account for a sizeable portion of phenotypic variance

Experience-dependent plasticity in adulthood
• challenges, physical activity structural changes in task-relevant areas
• According to one model (9), plastic changes are elicited by a mismatch between environmental demand and organismic supply, provided that the organism possesses the potential for a plastic response.
• distinction between plasticity and flexibility
• flexibility= capacity for variations in behavioral repertoire that do not require reorganization of brain structures and connections, plasticity= does
• older adults have a richer model of the world that enables deployment of established behavioral repertoires less plasticity
• cognitive interventions may ameliorate the course of cognitive aging but also suggest that plasticity decreases from early to late adulthood
The increasing importance of environmental support
• Memory performance is particularly impaired when retrieval depends on self-generated cues and active control processes
• Self-initiated processing and constructive cue generation require maintenance of task representations through recurrent connections between prefrontal and more posterior brain regions
• ability to hold task representations in mind declines with age
• older adults tend to rely more on external information than younger adults do
• but removal of environment not always bad, sometimes beneficial
• The tendency of older adults, both automatic and deliberate, to outsource control to the environment may be inefficient at times but cost effective in the long run if the cuing structure of the environment corresponds to their goals and needs
Mechanisms of successful cognitive aging
• assistive adaptive technology bad and good
Maintenance
• youth like brain structure= better cognitive performance
Compensation
• structural or functional reorganization
• more normal for damaging events, not aging
• although the frontal lobes are increasingly needed, they are decreasingly able to counteract the adverse consequences of senescence on sensory, perceptual, and motor aspects of behavior
Selection
• young can to task in more ways than one
• the more ways, the more alternatives in old age

Outlook
• cognitive development in adults= individual
• beneficial lifestyle choices
• medial temporal and prefrontal regions of the brain contribute differently to working memory and episodic memory in childhood and old age, presumably because medial-temporal lobe maturation progresses more rapidly than that of the frontal lobes, whereas both regions of the brain show signs of decline with advancing adult age