MEMORY MECHANISMS IN AGING, PRECLINICAL AND EARLY DEMENTIA

  • Sliwinski, Martin John (PI)
  • Lipton, Richard (PI)
  • Buschke, Herman (PI)
  • Lipton, Richard (PI)
  • DICKSON, DENNIS WILLIAM (PI)
  • CRYSTAL, HOWARD (PI)
  • Lee, Sunhee (PI)

Project: Research project

Project Details

Description

Because memory impairment is often the earliest effect of Alzheimer's
disease (AD), dementia-related memory impairment must be detected and
discriminated from aged related memory change. Long-term objectives are to
distinguish memory changes in aging and early AD, detect preclinical and
early AD, and validate criteria for diagnosis of preclinical AD. Specific
aims are to: 1) improve prediction of clinical AD by detecting specific
kinds of memory impairment in preclinical AD (i.e., encoding specificity)
that are not secondary to decline of more basic cognitive abilities (e.g.,
processing speed); 2) distinguish memory and cognitive changes due to
healthy aging from the memory and cognitive impairment due to preclinical
AD; 3) test the hypothesis that unrecognized preclinical AD contributes to
estimates of age-related cognitive decline in presumably non-demented
adults; and 4) to determine if the mediators of cross-sectional age
differences also mediate longitudinal cognitive decline in individuals.
Our specific hypothesis are that: 1) identification of preclinical AD can
be improved by detecting specific memory deficits in encoding specificity;
2) Preclinical AD will account for a significant amount of apparent age-
related variance in cognitive measures; 3) Individual differences in
processing speed and other basic mediators will account for cross-
sectional age differences; 4) There will be a direct relation between age
and encoding specificity that is not mediated by processing speed; 5)
Mediators of age-related cognitive differences will not account for the
cognitive differences related to preclinical AD; 6) Intra-individual age-
related decline in basic cognitive abilities will predict intra-individual
decline in memory, but 7) Significant longitudinal age-related decline in
memory will remain after accounting for status and change in processing
speed and other power mediators of cross-sectional age differences.
Regression analysis and structural modeling will be used to explain memory
changes in aging and AD by impairment of other cognitive processes in
tests of memory, encoding specificity, processing speed, verbal ability,
processing capacity, attention, and executive function. The results will
provide information needed to detect preclinical AD and predict clinical
AD, discriminate age-from AD-related cognitive changes, investigate
cognitive aging without dementia, provide early treatment of AD, and
correlate cognitive, physiologic, biochemical, neuropathologic, and
neuroimaging changes in aging and AD.
StatusFinished
Effective start/end date10/1/976/30/99

Funding

  • National Institute on Aging

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