2: aging + cogn Flashcards
research on human brain + cogn aging focuses on?
description, explanation, and potential intervention regarding changes, transitions and statuses in the human life span
research on human brain + cogn aging: all ___? (5)
levels (biochemical, cogn, behavioural, etc.), directions (gains/growth, maintenance, decline, degeneration), periods (ST, LT, transitional), rates of change, endpoints
4 ways of exploring/testing conditions/influences of brain/aging
observational. mechanism (animal models + experimental). epidemiological. clinical trials
4 phenotypes of brain + cogn aging? differentiated by?
normal/non-demented cognitive aging NA. mild cognitive impairment MCI. neurodegenerative disease NDD. health brain + cogn aging HBA. differentiaed by aging trajectories and clinical outcomes
what do you see with NAA
“normal”: maintenance and typical decline. graph: three lines where you can stay the same, have a little bit of improvement, or a shallow decline
what do you see with MCI
at risk state, potentially transitional to AD. baseline lower, and see maintenance or decline
what do you see with NDD
AD, dementia: baseline even lower, and you see a decline
what do you see with HBA?
sustained or exceptional levels in late life. overall line higher, and see maintenance + slight decline
2 types of AD? main cause?
familial, early onset AD: mutation causes an abnormal APP to be produced; inevitable but rare. sporaid/late onset AD: associated with genes and risk factors
most prominent genetic risk factor for AD? protection?
APOE E4: occurs in about 40% of AD patients. protection: APOE E2.
AD: prognosis? survival?
inevitable cognitive and health decline. 3 - 10 years
female vs. male AD?
incidence more prominent in women than in men
def: incidence vs. prevalance
I: number of NEW cases per year. P: TOTAL number of cases in a population
early changes: NA + preclnical AD: time frame? main anatomical changes?
5, 10, 20 years. entorhinal and hippocampal atrophy (memory problems) + ventricles enlarge
early changes: NA + preclnical AD: detection?
difficult to identify except informally + retrospectively or sometimes post mortem. could begin 10 - 20 years before clinically detectable signs of memory failure
preclinical AD with NA brain: concurrent differences? longitudinal trajectories?
concurrent differences intially not striking in any easily detectable morphological characteristic. trajectory: both follow gradual decline functions, over time preAD is more preciptous
5 changes in NA and pre-AD brain that are similar/overlapping?
shrinkage in hippocampus and PFC. degradation in white matter. vascular changes (narrowing vessels + fewer new capillaries). plaques + tangles. increase in inflammation.
what is the first classifiable phase?
mild cognitive impairment: the suspected precursor developmental phase between NA + AD; differentiates normal decline from NDD
what do you see with MCI (graphs?) goal for studying MCI? attribute bifurcation of trajectories to?
group differences but overlapping distributions. attributes bifurcation of trajectories to AD risk factors like genetics, enviro, lifestyle. goal: search for distinguishing and early markers + risk factors
