Publications by authors named "Fabian Limani"
Article Synopsis
- Midbrain dopamine neurons loss is a key feature of Parkinson's disease (PD), and the protein α-synuclein is linked to this condition but its role in neuronal vulnerability is unclear.
- Researchers developed a new viral vector to selectively overexpress human α-synuclein in specific neuron types, particularly focusing on dopamine neurons in the substantia nigra pars compacta (SNc).
- Increased levels of α-synuclein led to some pathological changes but surprisingly resulted in greater dopamine activity without causing neurodegeneration in these neurons over a 90-day period.
Loss of select neuronal populations such as midbrain dopamine (DA) neurons is a pathological hallmark of Parkinson's disease (PD). The small neuronal protein α-synuclein has been related both genetically and neuropathologically to PD, yet how it contributes to selective vulnerability remains elusive. Here, we describe the generation of a novel adeno-associated viral vector (AAV) for Cre-dependent overexpression of wild-type human α-synuclein.
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