The Role of Neuronal Membranes Deterioration in The Pathogenesis of Alzheimer’s Disease: An Ultrastructural Perspective

Abstract

Senile dementia of the Alzheimer’s type (SDAT) is diagnosed on the basis of well known histopathological alterations which are present, but at a much lesser extent, also in the brain of normal aged people. Since the difference seems to be only quantitative, some authors support the contention that subtle neurochemical alterations accumulate in the brain of old individuals and may ultimately show a clinically evident pathology (Roth, 1985; Arendt and Bigl, 1987; Bertoni-Freddari, 1988a). Cellular membranes, while being important permeability barriers, are also directly involved in several important processes such as active transport of molecules, hormonal and immunological stimulation, transmission of the nervous impulse, etc.. During aging, changes in membrane basic constituents (phospholipids, cholesterol and proteins) lead to impaired cellular performances and this fact appears to be particularly true for the membranes of postmitotic cells, like neurones, which have the same age of the organism to which they belong (Oestreicher et al., 1986). In nerve cells a proper substitution of damaged molecules at their membranes is a necessary prerequisite to preserve specific functions such as ion homeostasis and action potentials, thus any delay and/or mistake in the turnover of altered constituents of neuronal membrane may result in serious impairments of cellular performances and in a potential threat to nerve cell longevity. In the present paper we report the results of a quantitative morphometric study undertaken to seek changes in synaptic membranes and mitochondria during physiological aging and SDAT.