title: Protein homeostasis, aging and Alzheimer's disease.
abstract: Alzheimer's disease (AD) is one key medical challenge of the aging society and despite a great amount of effort and a huge collection of acquired data on molecular mechanisms that are associated with the onset and progression of this devastating disorder, no causal therapy is in sight. The two main hypotheses of AD, the amyloid cascade hypothesis and the Tau hypothesis, are still in the focus of AD research. With aging as the accepted main risk factor of the most important non familial and late onset sporadic forms of AD, it is now mandatory to discuss more intensively aspects of cellular aging and aging biochemistry and its impact on neurodegeneration. Since aging is accompanied by changes in cellular protein homeostasis and an increasing demand for protein degradation, aspects of protein folding, misfolding, refolding and, importantly, protein degradation need to be linked to AD pathogenesis. This is the purpose of this short review.
authors.affiliation: Institute for Pathobiochemistry, University Medical Center of the Johannes Gutenberg University, Duesbergweg 6, 55099 Mainz, Germany.
authors.forename: Tobias
authors.initials: T
authors.lastname: Morawe
authors.forename: Christof
authors.initials: C
authors.lastname: Hiebel
authors.forename: Andreas
authors.initials: A
authors.lastname: Kern
authors.forename: Christian
authors.initials: C
authors.lastname: Behl
mesh_terms: D000375:Aging / Q000378:metabolism* / Q000473:pathology*; D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology*; D006706:Homeostasis; D006801:Humans; D018832:Molecular Chaperones / Q000378:metabolism; D017510:Protein Folding; D011506:Proteins / Q000737:chemistry / Q000378:metabolism*; D059748:Proteolysis
chemical_list: D018832:Molecular Chaperones; D011506:Proteins