Abstract

Various methods for active or passive immunization are being pursued actively as potential therapies for several neurodegenerative diseases characterized by the accumulation of misfolded proteins, such as Alzheimer’s and Huntington’s diseases. Masliah and colleagues now provide the first evidence that this approach could also be applicable to synucleopathies, including Parkinson’s disease and dementia with Lewy bodies, in which insoluble forms of α-synuclein aggregate in characteristic cytoplasmic inclusions. Although limited to mouse models, the evidence provided opens up the possibility that anti-α-synuclein antibodies may counteract the neurotoxic effects of excess α-synuclein by promoting the degradation of these aggregates. If applicable to humans, this approach could provide a way to slow down the neurodegenerative process in patients with various forms of synucleopathies, including Parkinson’s disease.

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