alpha-synuclein


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alpha-synuclein

(ăl′fə-sĭ-no͞o′klē-ĭn, -nyo͞o′-)
n.
A polypeptide protein found primarily in brain neurons but seen also in the fibrils in Parkinson's disease, in the amyloid plaques of Alzheimer's disease, and in brain tissue affected by other neurodegenerative diseases.

SNCA

A gene on chromosome 4q21 that encodes alpha synuclein, which may be involved in regulating dopamine release and transport. SNCA induces fibrillisation of microtubule-associated protein tau, reduces neuronal responsiveness to apoptotic stimuli, and downregulates caspase-3.
References in periodicals archive ?
This protein plays multiple roles in the body; DJ-1 acts as an antioxidant, protecting neurons from oxidative stress, and has also been linked to prevent accumulation of alpha-synuclein (Tan & Skipper, 2007).
That study showed that about 60% of cells in specific skin structures in patients with Parkinson's disease had alpha-synuclein inclusions.
Current scientific understanding is that Parkinson's as well as MSA is caused by deposits of pathological forms of alpha-Synuclein in the nervous system.
Now trials are looking at whether an alpha-synuclein blood test could be the early warning sign doctors hope for.
A hallmark pathology of Parkinson's disease is aggregates of protein - chiefly alpha-synuclein - called Lewy bodies that accumulate in brain cells, leading to cell degeneration and cell death.
Oral administration of rotenone using a gavage and image analysis of alpha-synuclein inclusions in the enteric nervous system.
In Parkinson's the alpha-synuclein protein goes wrong, in Alzheimer's it's amyloid and tau, in Huntington's it's the Huntington protein.
Parkinson's disease is caused by a protein known as alpha-synuclein, which forms aggregates within neurons, killing them eventually.
Prof Omar and his team undertook the two-and-half-year long study titled 'The role of alpha-synuclein in Parkinson's disease: from molecular pathways in the disease to therapeutic approaches'.
Both alpha-synuclein and huntingtin are copper-binding proteins, and both have been associated with NMDA receptor-mediated neuronal toxicity.
Overexpression of a protein called alpha-synuclein appears to disrupt vital recycling processes in neurons, starting with their terminal extensions and working its way back to the cells' center, with the potential consequence of progressive degeneration and eventual cell death, declare researchers at the University of California, San Diego.
North Shore University Health System (North Shore) and Mayo Clinic researchers have partnered on a study that shows genetic and clinical evidence that therapies targeting the expression of alpha-synuclein, a gene whose function is involved in the development and progression of Parkinson's disease may accelerate disease progression and increase the risk of physical incapacitation and dementia.