Transgene Triggers Parkinsonian Neurodegeneration

 SELECTIVE DISAPPEARANCE: Compared to nontransgenic controls, transgenic (tg) mice that express human a-synuclein (SYN) show a loss of dopa-minergic terminals in the brain's basal ganglia, which include the striatum. In the half-decade after human a- synuclein (ha-syn) was discovered in amyloid plaques purified from brains of patients with Alzheimer,1 neuroscientists logically suspected that this synaptic protein played a role in Alzheimer disease. Codiscoverer Eliezer Masliah began to d

Douglas Steinberg
Oct 27, 2002
 SELECTIVE DISAPPEARANCE: Compared to nontransgenic controls, transgenic (tg) mice that express human a-synuclein (SYN) show a loss of dopa-minergic terminals in the brain's basal ganglia, which include the striatum.

In the half-decade after human a- synuclein (ha-syn) was discovered in amyloid plaques purified from brains of patients with Alzheimer,1 neuroscientists logically suspected that this synaptic protein played a role in Alzheimer disease. Codiscoverer Eliezer Masliah began to develop an ha-syn transgenic mouse in 1996 that he hoped would serve as an Alzheimer model.

Over the next two years, however, views about ha-syn underwent a radical makeover. Studies linked mutations in its gene to Parkinson disease and identified the protein in aggregates, known as Lewy bodies, which form inside neurons in Parkinson and other neurodegenerative disorders; ha-syn's role in Alzheimer disease appeared, in comparison, less compelling. Researchers began to envision...

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