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Pathological  -synuclein transmission initiated by binding lymphocyte-activation gene 3

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      Pathological α-synuclein transmission initiates Parkinson-like neurodegeneration in nontransgenic mice.

      Parkinson's disease is characterized by abundant α-synuclein (α-Syn) neuronal inclusions, known as Lewy bodies and Lewy neurites, and the massive loss of midbrain dopamine neurons. However, a cause-and-effect relationship between Lewy inclusion formation and neurodegeneration remains unclear. Here, we found that in wild-type nontransgenic mice, a single intrastriatal inoculation of synthetic α-Syn fibrils led to the cell-to-cell transmission of pathologic α-Syn and Parkinson's-like Lewy pathology in anatomically interconnected regions. Lewy pathology accumulation resulted in progressive loss of dopamine neurons in the substantia nigra pars compacta, but not in the adjacent ventral tegmental area, and was accompanied by reduced dopamine levels culminating in motor deficits. This recapitulation of a neurodegenerative cascade thus establishes a mechanistic link between transmission of pathologic α-Syn and the cardinal features of Parkinson's disease.
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        Staging of brain pathology related to sporadic Parkinson’s disease

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          Endosome maturation.

          Being deeply connected to signalling, cell dynamics, growth, regulation, and defence, endocytic processes are linked to almost all aspects of cell life and disease. In this review, we focus on endosomes in the classical endocytic pathway, and on the programme of changes that lead to the formation and maturation of late endosomes/multivesicular bodies. The maturation programme entails a dramatic transformation of these dynamic organelles disconnecting them functionally and spatially from early endosomes and preparing them for their unidirectional role as a feeder pathway to lysosomes.
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            Author and article information

            Journal
            Science
            Science
            American Association for the Advancement of Science (AAAS)
            0036-8075
            1095-9203
            September 29 2016
            September 29 2016
            : 353
            : 6307
            : aah3374
            10.1126/science.aah3374
            © 2016

            http://www.sciencemag.org/about/science-licenses-journal-article-reuse

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