NEUROPATHOLOGICAL CHANGES IN THE CEREBRAL-CORTEX OF 1258 CASES FROM AGERIATRIC HOSPITAL - RETROSPECTIVE CLINICOPATHOLOGICAL EVALUATION OF A 10-YEAR AUTOPSY POPULATION
P. Giannakopoulos et al., NEUROPATHOLOGICAL CHANGES IN THE CEREBRAL-CORTEX OF 1258 CASES FROM AGERIATRIC HOSPITAL - RETROSPECTIVE CLINICOPATHOLOGICAL EVALUATION OF A 10-YEAR AUTOPSY POPULATION, Acta Neuropathologica, 87(5), 1994, pp. 456-468
To examine the neuropathological and clinical characteristics of,cereb
ral aging, we evaluated retrospectively a non-selected autopsy populat
ion of 1258 patients from the Geriatric Hospital of the University of
Geneva School of Medecine. The prevalence of Alzheimer's disease incre
ased with age below 90 years of age. In the nonagenarians and centenar
ians, there was a decline in the number of affected cases. The distrib
ution with age of neurofibrillary tangles and senile plaques varied am
ong the cortical areas studied. The CA1 field of the hippocampus and t
he inferior temporal cortex displayed increasing densities of neurofib
rillary tangles with age, whereas the superior frontal and the occipit
al cortex were relatively spared, especially in patients in their tent
h and eleventh decade. The percentage of cases presenting with senile
plaques in the neocortex and hippocampal structure increased with age
with a marked predominance of cases with moderate to high senile plaqu
e densities. Neurofibrillary tangles were often observed in the CA1 fi
eld and the inferior temporal cortex of non-demented individuals and w
ere present in most cases with Alzheimer's disease. Conversely, the in
volvement of the superior frontal and occipital cortex was moderate ev
en in demented patients. The distribution of senile plaques was homoge
neous in all of the neocortical areas independently of the clinical di
agnosis. Moreover, there was no correlation between the presence of ne
urofibrillary tangles and senile plaques in the cerebral regions studi
ed. These results indicate a differential topography of neurofibrillar
y tangles and senile plaques, and suggest that overt clinical signs of
Alzheimer's disease are linked to the progression of the neurodegener
ative process in neocortical areas.