Literature DB >> 9024330

Neurobiology of Alzheimer's disease.

E R Peskind1.   

Abstract

Although the specific process that destroys neurons in patients with Alzheimer's disease (AD) remains obscure, biochemical studies of AD neurohistologic lesions and molecular attempts to map and clone genes in familial AD have contributed greatly to our knowledge of AD. The major component of the extraneuronal neuritic plaque is beta-amyloid (A beta), which may be neurotoxic. The major component of the intraneuronal neurofibrillary tangle is hyperphosphorylated tau protein. It is unclear why this process damages the neuronal cytoskeleton Familial AD is genetically heterogeneous. Chromosomes 21, 14, and 1 are causative genes in early-onset familial AD. The apolipoprotein E4 allele of chromosome 19 is a risk factor for both early- and late-onset AD. Unraveling the actions of these three causative genes and the apolipoprotein E4 allele may explain disease mechanisms common to all patients with AD.

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Year:  1996        PMID: 9024330

Source DB:  PubMed          Journal:  J Clin Psychiatry        ISSN: 0160-6689            Impact factor:   4.384


  3 in total

1.  Humanin decreases mitochondrial membrane permeability by inhibiting the membrane association and oligomerization of Bax and Bid proteins.

Authors:  Ze-Wei Ma; Dong-Xiang Liu
Journal:  Acta Pharmacol Sin       Date:  2017-12-21       Impact factor: 6.150

Review 2.  EFAD transgenic mice as a human APOE relevant preclinical model of Alzheimer's disease.

Authors:  Leon M Tai; Deebika Balu; Evangelina Avila-Munoz; Laila Abdullah; Riya Thomas; Nicole Collins; Ana Carolina Valencia-Olvera; Mary Jo LaDu
Journal:  J Lipid Res       Date:  2017-04-07       Impact factor: 5.922

3.  The neuroprotective functions of transforming growth factor beta proteins.

Authors:  Arpád Dobolyi; Csilla Vincze; Gabriella Pál; Gábor Lovas
Journal:  Int J Mol Sci       Date:  2012-07-03       Impact factor: 6.208

  3 in total

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