Role of alpha-synuclein and parkin in dopamine toxicity on SHSY5Y cells - Implications for sporadic parkinson's disease

By Rana Ranjitsinh R

Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by severe motor symptoms including uncontrollable tremor, postural imbalance, slowness of movement and rigidity [Lotharius and Brundin, 2002]. With the increase in lifespan of the general population there is a subsequent increase in the incidence and prevalence of this disease and it is becoming a significant socio-economic burden globally [Dowding et al., 2006].

Parkinson's disease manifests in both familial and sporadic forms. Familial forms of the disease results from mutations in various PD related genes, the most notable ones being α-synuclein and parkin. However, the steps from mutant gene to neurodegeneration is just beginning to be elucidated. The cause of sporadic PD which arises spontaneously is still not clear. A complex interplay between genetic and environmental factors seems to be responsible for the sporadic cases of PD [Kruger et al., 2002; Lansbury and Brice, 2002].

The major pathological hallmark of this disease is the loss of dopaminergic neurons in the substantia nigra which project into the striatum and results in a severe depletion of neurons in the striatum. Additional neuronal systems, including other catecholaminergic nuclei are also affected in the process [Lotharius and Brundin, 2002].

PD progression involves six neuropathological stages marked by the continuous development of Lewy bodies and Lewy neurites [Braak et al., 2004]. These intraneuronal inclusion bodies are mainly comprised of aggregations of the misfolded protein α-synuclein [Spillantini et al., 1997]. Among the several biochemical abnormalities associated with PD, mitochondrial.

• Format: Paperback
• Language: English
• ISBN: 1805251457
• ISBN13: 9781805251453
• Release Date: March 2023
• Publisher: Independent Author
• Length: 106 Pages
• Weight: 0.37 lbs.
• Dimensions: 0.3" x 6.0" x 9.0"