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Titolo:
Dysregulation of cellular calcium homeostasis in Alzheimer's disease - Badgenes and bad habits
Autore:
Mattson, MP; Chan, SL;
Indirizzi:
NIA, Gerontol Res Ctr 4F02, Neurosci Lab, Baltimore, MD 21224 USA NIA Baltimore MD USA 21224 tr 4F02, Neurosci Lab, Baltimore, MD 21224 USA Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA Johns Hopkins Univ Baltimore MD USA 21205 urosci, Baltimore, MD 21205 USA
Titolo Testata:
JOURNAL OF MOLECULAR NEUROSCIENCE
fascicolo: 2, volume: 17, anno: 2001,
pagine: 205 - 224
SICI:
0895-8696(200110)17:2<205:DOCCHI>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
AMYLOID-BETA-PEPTIDE; LIPID-PEROXIDATION PRODUCT; MITOCHONDRIAL PERMEABILITY TRANSITION; PROTECTS HIPPOCAMPAL-NEURONS; CORTICAL SYNAPTIC TERMINALS; NA+/K+-ATPASE ACTIVITY; ISCHEMIC BRAIN INJURY; METHYL-D-ASPARTATE; PRECURSOR PROTEIN; GLUTAMATE TRANSPORT;
Keywords:
amyloid; apoptosis; excitotoxicity; oxidative stress; presenilin; synaptic plasticity;
Tipo documento:
Review
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
185
Recensione:
Indirizzi per estratti:
Indirizzo: Mattson, MP NIA, Gerontol Res Ctr 4F02, Neurosci Lab, 5600 Nathan Shock Dr, Baltimore,MD 21224 USA NIA 5600 Nathan Shock Dr Baltimore MD USA 21224 e,MD 21224 USA
Citazione:
M.P. Mattson e S.L. Chan, "Dysregulation of cellular calcium homeostasis in Alzheimer's disease - Badgenes and bad habits", J MOL NEURO, 17(2), 2001, pp. 205-224

Abstract

Calcium is one of the most important intracellular messengers in the brain, being essential for neuronal development, synaptic transmission and plasticity, and the regulation of various metabolic pathways. The findings reviewed in the present article suggest that calcium also plays a prominent rolein the pathogenesis of Alzheimer's disease (AD). Associations between the pathological hallmarks of AD (neurofibrillary tangles [NFT] and amyloid plaques) and perturbed cellular calcium homeostasis have been established in studies of patients, and in animal and cell culture models of AD. Studies ofthe effects of mutations in the beta -amyloid precursor protein (APP) and presenilins on neuronal plasticity and survival have provided insight into the molecular cascades that result in synaptic dysfunction and neuronal degeneration in AD. Central to the neurodegenerative process is the inability of neurons to properly regulate intracellular calcium levels. Increased levels of amyloid beta -peptide (A beta) induce oxidative stress, which impairs cellular ion homeostasis and energy metabolism and renders neurons vulnerable to apoptosis and excitotoxicity. Subtoxic levels of A beta may induce synaptic dysfunction by impairing multiple signal transduction pathways. Presenilin mutations perturb calcium homeostasis in the endoplasmic reticulumin a way that sensitizes neurons to apoptosis and excitotoxicity; links between aberrant calcium regulation and altered APP processing are emerging. Environmental risk factors for AD are being identified and may include highcalorie diets, folic acid insufficiency, and a low level of intellectual activity (bad habits); in each case, the environmental factor impacts on neuronal calcium homeostasis. Low calorie diets and intellectual activity may guard against AD by stimulating production of neurotrophic factors and chaperone proteins, The emerging picture of the cell and molecular biology of AD is revealing novel preventative and therapeutic strategies for eradicating this growing epidemic of the elderly.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 18:37:23