Neuropathology of aging. Correlations with Alzheimer disease

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Article Title:	Neuropathology of aging. Correlations with Alzheimer disease
Authors:	Sorin Riga, Dan Riga, Aurel Ardelean, George Pribac, Anca Hermenean, Daniela Motoc, Francisc Schneider
Affiliation:	1 Department of Stress Research and Prophylaxis, ”Al. Obregia” Clinical Hospital of Psychiatry, Bucharest, Romania 2 ”Vasile Goldis” Western University, Arad, Romania
Abstract:	Introduction. The present study fills a gap in the Romanian bio-medical research domain through a global and unitary investigation of aging processes in the central nervous system (CNS) of both humans and animals, from macroscopic-regionalzonal levels to tissual-cellular-subcellular ones. In addition, the determination of correlations with Alzheimer disease (AD) has an important epistemological, biological, medical and therapeutic significance. Materials and methods. Human brains from elderly people (65 yrs. – 85 yrs.) and very elderly persons (85 yrs. and over), as well as aging CNS from mice, Wistar rats and guinea pigs were processed using macro- and microscopic morphological methods. Brain samples were investigated by light microscopy (histochemical stains and silver impregnation techniques), fluorescence and transmission electron microscopy. Neuropathological changes in aging brains were compared with brains of AD, prepared by the same methods and published in a previous paper. Results. By gross, imagistic and sectional anatomy, we evinced very gentle and/or mild to moderate macroscopic changes: cortical atrophy and ventricular dilatation, with gradual slow decline of brain weight and volume, modifications observed especially in elderly human CNS. By microscopic anatomy, histology and cytology we identified the main changes and markers of brain aging at tissual-cellular-subcellular levels: • mild reconfiguration of cyto- (neuron and glia), myelino- and lipopigmento- (LP – lipofuscin and ceroid) architectonics; • constant and abundant presence LP (lipopigments) as hallmark of cellular aging in the majority of neurons and glia (microglia, oligodendrocyte and astroglia); • moderate decrease of energetic system (mitochondria) and anabolic systems (hypoanabolism): polyribosomes • and rough endoplasmic reticulum (Nissl bodies) and Golgi apparatus, as well as moderate increase of lysosomal hidrolytic activity (hypercatabolism); • rare and diminished existence of specific AD neuropathological damages, seen in elderly and very elderly human brains, but much reduced in number, intensity and impairment; • mild increase of apoptosis and rare and isolated zones of necrosis, especially in human brain aging. Conclusions. The present study is the first Romanian research, in which aging processes of mammal brains were investigated from anatomo-histologico-tissual levels up to cellular-subcellular and extracellular impairments and in close connection with AD neuropathology. Results allow and prefigure new directions in approaching human longevity, sanogenesis, aging and treatment of age-related pathology.
Keywords:	cerebral senescence and Alzheimer disease, neuropathology and morphological correlations, selective and mild brain atrophy, reduction of neuron number and glial proliferation, increase of lipofuscin and ceroid pigments, decrease of Nissl bodies, diminished presence of Alzheimer neuropathology in aging brains
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*Correspondence:	Dan Riga, Department of Stress Research and Prophylaxis, ”Al. Obregia” Clinical Hospital of Psychiatry, 10 Berceni Rd., 041914 Bucharest 8, Romania, Tel. +40 21 334 3008, Fax +40 21 230 9579, email: D_S_Riga@yahoo.com