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Issue title: Tau and Beyond for Alzheimer's Disease: A Special Issue dedicated to Dr. Inge Grundke-Iqbal
Guest editors: Alejandra Alonso and Chengxin Gong
Article type: Review Article
Authors: Takashima, Akihiko; *
Affiliations: Department of Aging Neurobiology, National Center for Geriatrics and Gerontology, Oobu-shi, Aichi, Japan
Correspondence: [*] Correspondence to: Akihiko Takashima, Department of Aging Neurobiology, National Center for Geriatrics and Gerontology, 35 Gengo Morioka, Oobu-shi, Aichi, Japan. Tel.: +81 562 44 5651; Fax: +81 562 44 6597; E-mail: [email protected].
Abstract: Tauopathies are neurodegenerative diseases characterized behaviorally by dementia and neuropathologically by neurofibrillary tangles and neuronal loss. Tau gene mutations have been found in frontotemporal dementia with parkinsonism linked to chromosome 17, suggesting that mutation of tau induces tauopathy. Studies on in vitro tau aggregation show that tau forms two different intermediate aggregates—called tau oligomers and granular tau oligomers—before forming fibrils. Moreover, studies using a mouse model that expresses human tau demonstrated that the process of neurofibrillary tangle formation, rather than tangles themselves, may cause synapse loss and neuron loss. Further analyses suggest that hyperphosphorylated tau or oligomeric tau is involved in synaptic loss, whereas granular tau oligomers are responsible for neuronal loss. Thus, different forms of tau aggregates are involved in the different pathological changes that occur in tauopathies.
Keywords: Granular tau oligomer, neuron loss, synapse loss, tau fibril, tau oligomer
DOI: 10.3233/JAD-130653
Journal: Journal of Alzheimer's Disease, vol. 37, no. 3, pp. 565-568, 2013
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