Abstract
In a previous study of hippocampal neurons in aging and AD [Lancet 344 (1994) 769], we demonstrated that the loss of neurons in the CA1 region was disease-specific and not related to aging. In the present study, we examined for loss of hippocampal neurons in preclinical AD, a period during which there are abundant amyloid deposits in the brain but no evidence of cognitive decline. We examined the postmortem brains of 33 subjects from the Baltimore Longitudinal Study of Aging and the Johns Hopkins Alzheimer’s Disease Research Center. Using unbiased stereology, we estimated the total number of neurons in the granule cell layer, hilus, CA3-2, CA1, and subiculum of AD ( n=14), preclinical AD ( n=8), and age-matched control subjects ( n=11). The results from the present study confirm our previous finding of significant neuronal losses in the CA1 (48%), hilus (14%), and subiculum (24%) in AD [Lancet 344 (1994) 769]. However, we did not observe a significant loss of neurons in CA1 or any of the other subdivisions of the hippocampus in preclinical AD.
Highlights
Alzheimer’s disease (AD) is a progressive neurodegenerative disease characterized clinically by dementia and neurobehavioral deterioration [9,24]
In a previous study we described the pattern of loss of hippocampal neurons in normal aging and AD [39] and concluded that the most distinctive lesion of AD was the loss of neurons in the CA1 region
We used unbiased stereological techniques to examine the postmortem brains of subjects followed by the Baltimore Longitudinal Study of Aging (BLSA) and the Johns Hopkins University Alzheimer’s Disease Research Center (ADRC)
Summary
Alzheimer’s disease (AD) is a progressive neurodegenerative disease characterized clinically by dementia and neurobehavioral deterioration [9,24]. Not all of these pathological changes have been characterized before the onset of cognitive decline, i.e., in the preclinical stages of AD. The development of NFT and SP has been described in preclinical AD [25], but there is only a single stereological study of the number of neurons in the hippocampus in preclinical AD [26]. We found that the degeneration in CA1 was disease-specific and not related to aging, per se These findings have prompted us to examine whether or not a significant loss of hippocampal neurons, in particular in CA1, occurs in preclinical AD, that is, during a. In the present study, we extend our stereological evaluation of the number of hippocampal neurons to the preclinical stage of AD
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