J. Morys et al., THE 2ND LAYER NEURONS OF THE ENTORHINAL CARTER AND THE PERFORANT PATHIN PHYSIOLOGICAL AGING AND ALZHEIMERS-DISEASE, Acta Neurobiologiae Experimentalis, 54(1), 1994, pp. 47-53
The hippocampal formation was studied in 5 brains of younger (29 to 52
years of age) and 6 brains of elderly (61 to 89 years of age) subject
s without signs of dementia, as well as in 11 brains of patients with
Alzheimer's disease (65 to 91 years of age). The 8-mu m-thick sections
were stained either with cresyl violet, Well method or with immunocyt
ochemical methods for amyloid (4G8) and neurofibrillary tangles (Tau-1
). Cell bodies, senile plaques and tangles were counted in all brains.
In brains of patients with Alzheimer's disease a significant neuronal
loss (about 56%) was observed in the second layer of the entorhinal c
ortex. The tangles/neurones ratio was very high (62.79.1%) in this lay
er. A great number of senile plaques were present in the whole hippoca
mpal formation, especially in the molecular layer of the dentate gyrus
(22.91.5 plaques/mm(2)) which is the termination zone of the perforan
t path. It seems therefore, that pathological alterations in Alzheimer
's disease disrupt the main input to the hippocampal formation. In ''p
hysiological'' ageing we did not observe changes in the density of neu
rones, although single tangles and plaques were found in all hippocamp
al areas. In elderly individuals 3.81.3% of neurones of the second lay
er revealed neurofibrillary pathology; a few plaques were found in var
ious areas of the hippocampal formation. These observations may sugges
t only a slight decrease in number of neurones in the hippocampal form
ation. However, these changes cause a slight impairment of memory and
learning often found in elderly individuals without dementia.