P. Giannakopoulos et al., CEREBRAL-CORTEX PATHOLOGY IN AGING AND ALZHEIMERS-DISEASE - A QUANTITATIVE SURVEY OF LARGE HOSPITAL-BASED GERIATRIC AND PSYCHIATRIC COHORTS, Brain research reviews, 25(2), 1997, pp. 217-245
In order to explore the relationships between the involvement of speci
fic neuronal populations and cognitive deterioration, and to compare t
he hierarchical patterns of cortical involvement in normal brain aging
and Alzheimer's disease, over 1200 brains from elderly subjects witho
ut cognitive deficits, as well as from patients with age-associated me
mory impairment and Alzheimer's disease, were examined. Our results su
ggest that the neuropathological changes associated with normal brain
aging and Alzheimer's disease affect select cortical circuits at diffe
rent points in time. Extensive hippocampal alterations are correlated
with age-associated memory impairment, whereas substantial neurofibril
lary tangle formation in neocortical association areas of the temporal
lobe is a prerequisite for the development of Alzheimer's disease. De
spite several lines of evidence involving amyloid deposit in the patho
genesis of Alzheimer's disease and Down's syndrome, our observations i
ndicate that there is no correlation between senile plaque densities a
nd degree of dementia in both disorders. In contrast to younger elderl
y cases, in the ninth and tenth decades of life, there is a differenti
al cortical involvement in that parietal and cingulate areas are early
affected in the course of Alzheimer's disease, and neocortical senile
plaques densities are strongly correlated with the severity of dement
ia. Moreover, Alzheimer's disease symptomatology is characterized in t
hese very old patients by high neurofibrillary tangle densities in the
anterior CA1 field, but not in the entorhinal cortex and inferior tem
poral cortex. These observations are discussed in the light of the hyp
othesis of global corticocortical disconnection and with respect to th
e notion of selective neuronal vulnerability in Alzheimer's disease. (
C) 1997 Elsevier Science B.V.