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Parkinson's Disease: Mitochondrial Molecular Pathology, Inflammation, Statins, and Therapeutic Neuroprotective Nutrition
Author(s) -
Kones Richard
Publication year - 2010
Publication title -
nutrition in clinical practice
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.725
H-Index - 71
eISSN - 1941-2452
pISSN - 0884-5336
DOI - 10.1177/0884533610373932
Subject(s) - medicine , substantia nigra , neuroprotection , parkin , inflammation , parkinson's disease , microglia , coenzyme q10 , disease , lewy body , pharmacology , pathology , immunology
Pathological hallmarks of Parkinson's disease are destruction of dopaminergic neurons in the basal ganglia, especially the substantia nigra, and the presence of Lewy bodies within nerve cells. Environmental toxins are associated with the disease and, in a minority of cases, genetic factors have been identified. Inflammation—with activation of phagocytic microglia, release of cytokines, invasion by T cells, and complement activation—plays a role in damaging these neurons. Excessive production of reactive oxygen species, mitochondrial dysfunction leading to apoptosis, accumulation and oligomerization of the protein α‐synuclein, and defective protein disposal by the ubiquitin proteasome system are involved in the complex web of events mediating nigral cell demise. Two agents of current interest, coenzyme Q10 and creatine, may be disease modifying, and large studies are in progress. Related mechanisms of other substances, including ω‐3 fatty acids and vitamin D, are included in this review. The association with serum cholesterol levels and the effects of statin drugs are uncertain but important.