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P‐138: An autopsy‐confirmed case study of the conversion from normal cognition to amnestic MCI to AD
Author(s) -
Zec Ronald F.,
Burkett Nicole,
Markwell Stephen,
Moore Brian
Publication year - 2007
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2007.04.202
Subject(s) - dementia , psychology , entorhinal cortex , cognition , audiology , alzheimer's disease , verbal learning , neuropsychology , boston naming test , cognitive test , hippocampus , psychiatry , disease , clinical psychology , medicine , neuroscience , pathology
Background: The conversion from Mild Cognitive Impairment (MCI) to dementia has received considerable research attention, whereas the transition from normal cognition to MCI and dementia in an autopsy-confirmed case of Alzheimer disease (AD) has not been studied in detail. Objective: We studied the conversion from normal memory and cognition to MCI of the amnestic type to early dementia with annual assessments over 10 years using a comprehensive neuropsychological test battery in a neuropathologically-confirmed case of AD. Methods: The woman was 74 years old at the first evaluation and was 84 years old at the time of her last assessment. She was a retired high school teacher with 18 years of education. An annual half-day cognitive assessment was administered to the patient including tests of mental status, attention, new learning and memory, language, visuospatial functioning, and problem solving ability. Results: The patient scored well within normal limits on all memory and cognitive test measures using age norms at her first evaluation (age 74). A gradual progressive decline over ten years on measures of new declarative learning and memory, especially on word-list learning tests, was found resulting in severe memory impairment at age 78. Only later did measurable decline on the non-memory cognitive measures emerge. Neuropathological findings at autopsy revealed Alzheimer-type changes that indicated a high likelihood, by NIA-Reagan criteria, that the dementia was due to Alzheimer disease. There was moderate CERAD plaque grade and Braak and Braak tangle stage V. There was a heavy NFT and NP burden in the hippocampus, entorhinal cortex, perirhinal cortex, and amygdala, a moderate number in the inferior temporal gyrus with less Alzheimer pathology burden in the frontal, parietal, and occipital cortices and the superior temporal gyrus. Conclusions: Progressive memory decline in an autopsy-confirmed case of AD occurred gradually over 7-8 years before there is detectable nonmemory cognitive deficits emerged on a comprehensive neuropsychological battery of tests. This case is likely representative of many, but not all, cases of AD.

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