Abstract
Introduction and aim: Different acute and chronic experimental models mimick certain pathological hallmarks associated with Parkinson's disease (PD): while lesion models induce selectively a dopaminergic deficit in the nigrostriatal system, transgenic models lead to an accumulation of alpha-synuclein. In alpha-synuclein models wild-type alpha-synuclein accumulates during aging, whereas alpha-synuclein mutations (e.g. A53T) lead to an earlier onset as well as a more severe course of the disease. Accumulation of alpha-synuclein in the forebrain as well as in the olfactory bulb is particularly of clinical relevance, because olfactory dysfunction is one of the initial symptoms during the course of PD. More importantly, the olfactory bulb is one of the unique regions in the CNS characterized by a continuous generation of new neurons. Therefore, the aim of these consecutive studies was to analyze olfactory neurogenesis in different models of PD in the adult and during aging.
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