title: Alzheimer's Disease: Mechanism and Approach to Cell Therapy.
abstract: Alzheimer's disease (AD) is the most common form of dementia. The risk of AD increases with age. Although two of the main pathological features of AD, amyloid plaques and neurofibrillary tangles, were already recognized by Alois Alzheimer at the beginning of the 20th century, the pathogenesis of the disease remains unsettled. Therapeutic approaches targeting plaques or tangles have not yet resulted in satisfactory improvements in AD treatment. This may, in part, be due to early-onset and late-onset AD pathogenesis being underpinned by different mechanisms. Most animal models of AD are generated from gene mutations involved in early onset familial AD, accounting for only 1% of all cases, which may consequently complicate our understanding of AD mechanisms. In this article, the authors discuss the pathogenesis of AD according to the two main neuropathologies, including senescence-related mechanisms and possible treatments using stem cells, namely mesenchymal and neural stem cells.
authors.affiliation: Department of Neuroscience, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Videnska 1083, 142 20 Prague 4, Czech Republic. amemori@biomed.cas.cz.
authors.forename: Takashi
authors.initials: T
authors.lastname: Amemori
authors.affiliation: Department of Neuroscience, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Videnska 1083, 142 20 Prague 4, Czech Republic. jendel@biomed.cas.cz.|Department of Neuroscience, 2nd Faculty of Medicine, Charles University, V Uvalu 84, 150 06 Prague 5, Czech Republic. jendel@biomed.cas.cz.
authors.forename: Pavla
authors.initials: P
authors.lastname: Jendelova
authors.affiliation: Department of Neuroscience, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Videnska 1083, 142 20 Prague 4, Czech Republic. j.ruzicka@biomed.cas.cz.
authors.forename: Jiri
authors.initials: J
authors.lastname: Ruzicka
authors.affiliation: Department of Neuroscience, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Videnska 1083, 142 20 Prague 4, Czech Republic. urdzikl@biomed.cas.cz.
authors.forename: Lucia Machova
authors.initials: LM
authors.lastname: Urdzikova
authors.affiliation: Department of Neuroscience, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Videnska 1083, 142 20 Prague 4, Czech Republic. sykova@biomed.cas.cz.|Department of Neuroscience, 2nd Faculty of Medicine, Charles University, V Uvalu 84, 150 06 Prague 5, Czech Republic. sykova@biomed.cas.cz.
authors.forename: Eva
authors.initials: E
authors.lastname: Sykova
mesh_terms: D017668:Age of Onset; D000375:Aging / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D000544:Alzheimer Disease / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000628:therapy*; D016229:Amyloid beta-Peptides / Q000276:immunology / Q000378:metabolism; D000818:Animals; D064987:Cell- and Tissue-Based Therapy / Q000379:methods; D004195:Disease Models, Animal; D004734:Energy Metabolism; D006801:Humans; D007167:Immunotherapy / Q000379:methods; D009154:Mutation; D009457:Neuroglia / Q000378:metabolism; D058225:Plaque, Amyloid / Q000378:metabolism / Q000473:pathology; D033581:Stem Cell Transplantation / Q000379:methods; D013234:Stem Cells / Q000166:cytology / Q000378:metabolism; D016875:tau Proteins / Q000276:immunology / Q000378:metabolism
chemical_list: D016229:Amyloid beta-Peptides; D016875:tau Proteins
keywords: Alzheimer’s disease; Tau; amyloid-β; mesenchymal stem cells; neural stem cells