作者: Andres Kriete
DOI: 10.1007/978-1-4614-3411-5_3
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摘要: Parkinson’s disease (PD), like many other dementias, is a of old age with neurological-pathological signs and underlying molecular mechanisms that precede cell death. Deciphering PD specifically from an aging perspective has advantages. shares multiple aging, albeit in accelerated fashion, including accumulation damage dysfunction, stress responses, deficiencies the maintenance protein quality. Here, we review foundations new hybrid, phenotypical model, which combines organelle phenotypes associated long-term progression normal aging. Subsequently, adapt this model to demonstrate acceleration dysfunction. On level mechanisms, discuss two pathways play key role both PD: NF-κB mTOR. The introduction comprehensive modeling approaches expected make significant contribution deciphering relationship between different processes risks factors. In particular, tight as discussed here sheds light on future strategies for interventions.