The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
α-Syn suppression reverses synaptic and memory defects in a mouse model of dementia with Lewy bodies.
СтатьяПоддержка NIH: внешняя программаПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Lim Youngshin, Kehm Victoria M, Lee Edward B, Soper James H, Li Chi, Trojanowski John Q, Lee Virginia M-Y
Аннотация
Abnormally accumulated α-synuclein (α-syn) is a pathological hallmark of Lewy body-related disorders such as Parkinson's disease (PD) and dementia with Lewy body disease (DLB). However, it is not well understood whether and how abnormal accumulation of α-syn leads to cognitive impairment or dementia in PD and DLB. Furthermore, it is not known whether targeted removal of α-syn pathology can reverse cognitive decline. Here, we found that the distribution of α-syn pathology in an inducible α-syn transgenic mouse model recapitulates that in human DLB. Abnormal accumulation of α-syn in the limbic system, particularly in the hippocampus, correlated with memory impairment and led to structural synaptic deficits. Furthermore, when α-syn expression was suppressed, we observed partial clearing of pre-existing α-syn pathology and reversal of structural synaptic defects, resulting in an improvement in memory function.
Предметные рубрики MeSH
Acoustic StimulationAge FactorsAnalysis of VarianceAnimalsAnimals, NewbornBrainCalcium-Calmodulin-Dependent Protein Kinase Type 2Conditioning, ClassicalCuesDisease Models, AnimalDisease ProgressionEmbryo, MammalianFearFemaleGene Expression RegulationGlial Fibrillary Acidic ProteinGliosisHumansIn Vitro TechniquesIndolesLewy Body DiseaseMaleMemory DisordersMiceMice, Inbred C57BLMice, TransgenicMutationNerve DegenerationNerve Tissue ProteinsSerineSynapsesalpha-Synuclein