Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 22, Issue 14, Pages -Publisher
MDPI
DOI: 10.3390/ijms22147630
Keywords
Parkinson's disease; lipid metabolism; alpha-synuclein; GBA; LRRK2
Funding
- Fondazione Banco di Sardegna (Bando-2017-Iaccarino)
- Fondo di Ateneo per la ricerca 2019 Iaccarino
- Fondo di Ateneo per la ricerca 2019 Crosio
- PON 2014-2020 [CCI2014IT16M2OP005]
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Parkinson's disease is a complex neurodegenerative disorder with causes attributed to both genetic and environmental factors. Lipids play a significant role in the pathological pathways of PD, potentially contributing to neuronal toxicity through protein alterations.
Parkinson's disease (PD) is a complex and progressive neurodegenerative disorder with a prevalence of approximately 0.5-1% among those aged 65-70 years. Although most of its clinical manifestations are due to a loss of dopaminergic neurons, the PD etiology is largely unknown. PD is caused by a combination of genetic and environmental factors, and the exact interplay between genes and the environment is still debated. Several biological processes have been implicated in PD, including mitochondrial or lysosomal dysfunctions, alteration in protein clearance, and neuroinflammation, but a common molecular mechanism connecting the different cellular alterations remains incompletely understood. Accumulating evidence underlines a significant role of lipids in the pathological pathways leading to PD. Beside the well-described lipid alteration in idiopathic PD, this review summarizes the several lipid alterations observed in experimental models expressing PD-related genes and suggests a possible scenario in relationship to the molecular mechanisms of neuronal toxicity. PD could be considered a lipid-induced proteinopathy, where alteration in lipid composition or metabolism could induce protein alteration-for instance, alpha-synuclein accumulation-and finally neuronal death.
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