SCImago Journal & Country Rank

Ranking and Indexing

Rank:
Index Copernicus Value (2010): 5.45
CNCSIS B+ (code 820) since 2007

International Databases:
SCOPUS since 2009
EBSCO Academic Search Complete since 2008
Index Copernicus Journals Master List since 2009
Directory of Open Access Journals (DOAJ) since 2008
ProQuest
Genamics JournalSeek since 18/2008

International Catalogues:
Oxford University's Library since 2003

Journal Info

Title: Studia Universitatis Vasile Goldis, Seria Stiintele Vietii (Life Sciences Series)
Abbreviated title: Studia Univ. VG, SSV
Publisher: "Vasile Goldis" University Press
Owner: Western University "Vasile Goldis" Arad, Romania
ISSN: 1584-2363
e-ISSN: 1842-7863
ISSN-L: 1584-2363

Who's Online

We have 42 guests online

Index Databases

Neuropathology of aging. Correlations with Alzheimer disease Print E-mail
Written by Riga S., Riga D., Ardelean A., Pribac G., Hermen   
Read full article
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
References: Abraham CR. Amiloid b peptide: a century of discoveries. Amyloid: Int J Exp Clin Invest. 2000; 7:7-9.
Abraham CR, Slot F. Metalloendopeptidase EC 3.4.24.15 in neurodegeneration. In: A. Lajtha, N.L. Benik (eds). Role of Proteases in the Pathophysiology of Neurodegenerative Diseases. Kluwer/Plenum, New York, NY, 2001: 101-116.
American Psychiatric Association. DSM-IVTR. Diagnostic and Statistical Manual of Mental Disorders. Forth Edition Text Revision. American Psychiatric Association, Washington, DC, 2000.
Ames BN, Shigenaga MK, Hagen TM. Oxidants, antioxidants, and degenerative diseases of aging. Proc Natl Acad Sci USA. 1993; 90:7915-7922.
Beckman KB, Ames BN. The free radical theory of aging matures. Physiol Rev. 1998; 78:547-581.
Bi X, Zhou J, Lynch G. Lysosomal protease inhibitors induce meganeurites and tanglelike structures in entorhinohippocampal regions vulnerable to Alzheimer’s disease. Exp Neurol. 1999; 158: 312-327.
Braak H. Architectonics as seen by lipofuscin stains. In: A. Peters, E.G. Jones eds. Cerebral Cortex, vol. 1. Plenum, New York, NY, 1984: 59-104.
Braak H, Braak E, Morphology of the human isocortex in young and aged individuals: qualitative and quantitative findings, In: J. Ulrich (ed.), Histology and Histopathology of the Aging Brain (H. P. von Hahn, ed., Interdisciplinary Topics in Gerontology, vol. 25), Karger, Basel, CH, 1988: 1-15.
Brunk UT, Terman A. The mitochondrial-lysosomal axis theory of aging. Accumulation of damaged as a result of imperfect autophagocytosis. Eur J Biochem. 2002; 269:1996-2002.
Cervós-Navarro J, Sarkander H-I (eds). Brain Aging: Neuropathology and Neuropharmacology. Raven Press, New York, NY, 1983.
Delhalle S, Duvoix A, Schnekenburger M, Morceau F, Dicato M, Diederich M. An introduction to the molecular mechanisms of apoptosis. Ann NY Acad Sci. 2003; 1010:1-8.
Evans PH. Free radicals in brain metabolism and pathology. Br Med Bull. 1993; 49:577-587.
Finch CE, Rozovsky I, Stone D, Morgan TE. Glial activitation during aging in the rat brain: gene expression and proliferative potential. In: VA Bohr, BFC Clark, T. Stevnsner (eds), Molecular Biology of Aging, Munksgaard, Copenhagen, DK. Alfred Benzon Symposium; 1999; 44:304-315.
Fosslien E. Mitochondrial medicine-molecular pathology of defective oxidative phosphorylation. Ann Clin Lab Sci. 2001; 31:25-67.
Glees P, Hasan M. Lipofuscin in Neuronal Aging and Diseases. Georg Thieme, Stuttgart, DE, 1976.
Gonzáles-Scarano F, Baltuch G. Microglia as mediators of inflammatory and degenerative diseases. Annu Rev Neurosci, 1999; 22: 219-240.
Grune T, Jung T, Merker K, Davies KJA. Decreased proteolysis caused by protein aggregates, inclusion bodies, plaques, lipofuscin, ceroid, and “aggresomes” during oxidative stress, aging, and disease. Int J Biochem Cell Biol. 2004; 36: 2519-2530.
Harman D. Free radical involvement in aging. Pathophysiology and therapeutic implications. Drugs and Aging, 1993; 3: 60-80.
Harman D. Free radical theory of aging. In: Klatz R, Goldman R, eds. The Science of Anti-Aging
Medicine, 2003 Update. American Academy of Anti-Aging Medicine (A4M), Chicago, IL, 2003: 15-31.
Hayat MA. Principles and Techniques of Electron Microscopy, vol. 1. Van Nostrand Reinhold, New York, NY, 1970.
Keck S, Nitsch R, Grune T, Ullrich O. Proteasome inhibition by paired helical filament-tau in brains of patients with Alzheimer’s disease. J Neurochem, 2003; 85:115-122.
Landfield PW, Baskin RK, Pitler TA. Brain aging correlates: retardation by hormonalpharmacological treatments. Science. 1981; 214:581-584.
Lynch G, BI X. Lysosomes and brain aging in mammals. Neurochem Res. 2003; 28:1725-1734.
Marinesco G, La cellule nerveuse, vol. 1 et vol. 2, Octave Doin et Fils Éd., Paris, FR, 1909.
McKhann G, Drachman D, Folstein M, Katzman R, Price D, Stadlan EM. Clinical diagnosis of Alzheimer’s disease: report of the NINCDSADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer’s Disease. Neurology, 1984; 34: 939-944.
Morgan TE, Xie Z, Goldsmith S, Yoshida T, Lanzrein A-S, Stone D, Rozovsky I, Perry G, Smith MA, Finch CE. The mozaic of brain glial hyperactivity during normal ageing and its attenuation by food restriction. Neuroscience, 1999; 3: 687-699.
Nandy, K. Properties of neuronal lipofuscin pigment in mice. Acta Neuropathol. (Berl.), 1971; 19: 25-32.
Porta EA. Advances in age pigment research. Arch Gerontol Geriatr, 1991; 12:303-320.
Riga S, Riga D. Effects of centrophenoxine on the lipofuscin pigments in the nervous system of old rats. Brain Res, 1974; 72: 265-275.
Riga S, Riga D. Antagonic-Stress: a therapeutic composition for deceleration of aging. I. Brain lipofuscinolytic activity demonstrated by light and fluorescence microscopy. Arch. Gerontol. Geriatr, 1994a; 19(S4): 217-226.
Riga D, Riga S. Antagonic-Stress: a therapeutic composition for deceleration of aging. II. Brain lipofuscinolytic activity demonstrated by electron microscopy. Arch. Gerontol. Geriatr, 1994b; 19(S4): 227-234.
Riga D, Riga S. Lipofuscin and ceroid pigments in aging and brain pathology. A review. I. Biochemical and morphological properties. Rom J Neurol Psychiat, 1995a; 33:121-136.
Riga S, Riga D. An antistress and antiaging neurometabolic therapy: accelerated lipofuscinolysis
and stimulated anabolic regeneration by the Antagonic-Stress synergistic formula. Ann NY Acad Sci. 1995b; 771: 535-550.
Riga D, Riga S, Schneider F. Regenerative medicine: Antagonic-Stress® therapy in distress and aging. I. Preclinical synthesis - 2003. Ann NY Acad Sci, 2004; 1019: 396-400.
Riga D, Riga S, Hălălău F, Schneider F. Lipofuscin and ceroid pigments - markers of normal and pathological brain aging, pp. 213-221. In: R. Klatz, R. Goldman (eds), Anti-Aging Therapeutics, vol. 8, American Academy of Anti-Aging Medicine (A4M), Chicago, IL, 2006.
Riga D, Riga S, Ardelean A, Hermenean A, Schneider F. Leziuni neuro-degenerative în boala Alzheimer şi în patologia asociată îmbătrânirii. A 27-a Sesiune Ştiinţifică Anuală a Societăţii Române de Biologie Celulară, Bistriţa, 11-14 iunie, 2009; Buletinul Societăţii Române de Biologie Celulară, 37: 25, 2009a.
Riga S, Riga D, Hermenean A, Ardelean A, Schneider F. Modificări neuro-degenerative în îmbătrânire. A 27-a Sesiune Ştiinţifică Anuală a Societăţii Române de Biologie Celulară, Bistriţa, 11-14 iunie, 2009; Buletinul Societăţii Române de Biologie Celulară, 37: 26, 2009b.
Riga D, Riga S, Ardelean A, Pribac G, Schneider F. Neuropathology of Alzheimer disease. Connexions with cerebral senescence. Studia Universitatis Vasile Goldis. Life Sciences Series, 21(1), 2011, in press. Rush Jr AJ, First MB, Blacker D (eds). Handbook of Psychiatric Measures, 2nd ed. American Psychiatric Publ, Washington, DC, 2008.
Samorajski T, Keefe JR, Ordy, JM. Intracellular localization of lipofuscin age pigments in the nervous system. J Gerontol, 1964; 19: 262-276.
Terman A, Brunk UT. Lipofuscin: Mechanisms of formation and increase with age. APMIS, 1998; 106: 265-276.
Terman A. Garbage catastrophe theory of aging: imperfect removal of oxidative damage? Redox Rep, 2001; 6: 15-26.
Terman A, Brunk UT. Aging as a catabolic malfunction. Int J Biochem Cell Biol, 2004; 36: 2365-2375.
Thompson SW, Hunt RD. Selected Histochemical and Histopathological Methods. Charles C. Thomas, Springfield, IL, 1966.
World Health Organization. The ICD-10 Classification of Mental and Behavioural Disorders. Clinical Descriptions and Diagnostic Guidelines. World Health Organization, Geneva, CH, 1992.
*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: This e-mail address is being protected from spambots. You need JavaScript enabled to view it