Where is alpha-synuclein located?

Where is alpha-synuclein located?

Alpha-synuclein is abundant in the brain, and smaller amounts are found in the heart, muscles, and other tissues. In the brain, alpha-synuclein is found mainly at the tips of nerve cells (neurons) in specialized structures called presynaptic terminals.

Does alpha-synuclein cause PD?

α-Synuclein may contribute to PD pathogenesis in a number of ways, but it is generally thought that its aberrant soluble oligomeric conformations, termed protofibrils, are the toxic species that mediate disruption of cellular homeostasis and neuronal death, through effects on various intracellular targets, including …

How does alpha-synuclein cause Parkinson’s?

PD is characterized by the loss of dopaminergic neuronal cells in the substantia nigra pars compacta and the abnormal accumulation and aggregation of α-Syn in the form of Lewy bodies and Lewy neurites. More precisely, the aggregation of α-Syn is associated with the dysfunctionality and degeneration of neurons in PD.

Where are Lewy bodies found?

Lewy bodies (LBs)are found throughout the brain stem, limbic and neocortical areas in Parkinson’s disease.

What causes alpha-synuclein buildup?

In Parkinson’s, the neurons’ normal processes for discarding waste may be faulty, so toxic substances can build up – including clumping alpha-synuclein. Up to 10% of people with Parkinson’s carry a fault in the GBA-1 gene, which is involved in cellular waste removal.

Why does alpha-synuclein cause disease?

Alpha-synuclein accumulation In Parkinson’s however, it misfolds and aggregates into clumps called Lewy Bodies. It’s thought these may be toxic and the aggregates of alpha-synuclein may also get passed from one neuron to another, causing the spread of the disease through the brain.

How do I lower my alpha-synuclein?

Reducing aggregation can be achieved by impeding the multimerization of α-syn through heat shock proteins (HSPs) for example, or by dissociating existing aggregates with small molecules. Blocking α-syn entry through receptor blocking would directly target the spread of α-syn and prevent its transport from cell to cell.