Open AccessDysfunction of mitochondria as the basis of Parkinson’s disease
Author(s) -
Małgorzata Popis
Publication year - 2018
Publication title -
medical journal of cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.294
H-Index - 8
ISSN - 2544-3577
DOI - 10.2478/acb-2018-0027
Subject(s) - substantia nigra , mitophagy , parkinson's disease , neuroscience , mitochondrion , disease , dopaminergic , oxidative stress , dopamine , proteostasis , biology , population , pathogenesis , medicine , genetics , pathology , endocrinology , autophagy , immunology , apoptosis , environmental health
Parkinson's disease is the second most common neurodegenerative disease, affecting about 0,15-0,3% of the world's population. Its characteristic feature is a loss of dopaminergic neurons in the substantia nigra. PD leads to dopamine deficiency and formation of intracellular inclusions called Lewy bodies, whose main ingredient is α-synuclein. Other types of nervous system cells are also affected by changes associated with that disease. The underlying molecular pathogenesis involves multiple pathways and mechanisms: mitochondrial function, oxidative stress, genetic factors, α-synuclein proteostasis, mitochondrial dynamic impairment, and disorders of the mitophagy process. This review summarizes the factors affecting the functioning of the mitochondria and their connection to the development of Parkinson's disease.