Injecting the abnormal protein associated with Parkinson's disease into the brains of mice causes key symptoms of the disorder, seemingly by spreading from one neuron to another. The findings point to a causal link between the misfolded protein, α-synuclein, and the neurodegeneration seen in Parkinson's.

Virginia Lee and her colleagues at the University of Pennsylvania in Philadelphia injected a synthetic abnormal form of α-synuclein into the mouse striatum, a brain region to which the neurons that die in Parkinson's project. The injected protein clumped together to form Lewy bodies, a signature of Parkinson's disease. Neurons then began to die, and neurons that link up with those near the injection site also developed Lewy bodies, indicating cell-to-cell transmission of α-synuclein. Six months after the injection, the animals' motor coordination, strength and balance had deteriorated — all Parkinsonian symptoms.

Antibodies against α-synuclein could stop or slow down the spread of the disease, the authors suggest.

Science 338, 949–953 (2012)