DISTINCT PATTERNS OF NEURONAL LOSS AND ALZHEIMERS-DISEASE LESION DISTRIBUTION IN ELDERLY INDIVIDUALS OLDER THAN 90 YEARS

Citation
P. Giannakopoulos et al., DISTINCT PATTERNS OF NEURONAL LOSS AND ALZHEIMERS-DISEASE LESION DISTRIBUTION IN ELDERLY INDIVIDUALS OLDER THAN 90 YEARS, Journal of neuropathology and experimental neurology, 55(12), 1996, pp. 1210-1220
Citations number
46
Categorie Soggetti
Pathology,Neurosciences,"Clinical Neurology
ISSN journal
00223069
Volume
55
Issue
12
Year of publication
1996
Pages
1210 - 1220
Database
ISI
SICI code
0022-3069(1996)55:12<1210:DPONLA>2.0.ZU;2-U
Abstract
To explore the characteristics of brain aging in very old individuals, we performed a quantitative analysis of neurofibrillary tangle (NFT) and senile plaque (SP) distribution and neuron densities in 13 nondeme nted patients, 15 patients with very mild cognitive impairment, and 22 patients with Alzheimer's disease (AD), all older than 96 years of ag e. Nondemented cases displayed substantial NFT formation in the CA1 fi eld and entorhinal cortex only. Very mild cognitive impairment cases w ere characterized by the presence of high NFT densities in layers V an d VI of area 20, and AD cases had very high NFT densities in the CA1 f ield compared to nondemented cases. Moreover, high SP densities were f ound in areas 9 and 20 in AD, but not in cases with very mild cognitiv e impairment and nondemented cases. In contrast to previous reports co ncerning younger demented patients, neuron densities were preserved in the CA1 field, dentate hilus, and subiculum in centenarians with AD. In these cases, there was a marked neuronal loss in layers II and V of the entorhinal cortex, and in areas 9 and 20. In the present series, no correlation was found between neurofibrillary tangle and neuron den sities in the areas studied, whereas there was a negative correlation between senile plaque and neuron densities in area 20. The comparison between the present data and those reported previously concerning youn ger cohorts suggests that there is a differential cortical vulnerabili ty to the degenerative process near the upper age-limit of life.