Abstract
Neurodegenerative diseases are usually sporadic in nature and commonly influenced by a wide range of genetic, life style and environmental factors. A unifying feature of Alzheimer's disease (AD) and Parkinson's disease (PD) is the abnormal accumulation and processing of mutant or damaged intra and extracellular proteins; this leads to neuronal vulnerability and dysfunction in the brain. Through a detailed review of ubiquitin proteasome, mRNA splicing, mitochondrial dysfunction, and oxidative stress pathway interrelation on neurodegeneration can improve the understanding of the disease mechanism. The identified pathways common to AD and PD nominate promising new targets for further studies, and as well as biomarkers. These insights suggested would likely provide major stimuli for developing unified treatment approaches to combat neurodegeneration. More broadly, pathways can serve as vehicles for integrating findings from diverse studies of neurodegeneration. The evidence examined in this review provides a brief overview of the current literature on significant pathways in promoting in AD, PD. Additionally, these insights suggest that biomarkers and treatment strategies may require simultaneous targeting of multiple components.
Original language | English |
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Pages (from-to) | 765-777 |
Number of pages | 13 |
Journal | Biomedicine & Pharmacotherapy |
Volume | 111 |
DOIs | |
Publication status | Published - 1 Mar 2019 |
Keywords
- alpha-synuclein
- alzheimer's disease
- biomarker
- dependent protein-degradation
- lewy bodies
- lipid-peroxidation
- mitochondrial dysfunction
- mrna splicing
- onset parkinsonism
- oxidative stress
- parkinson's disease
- traumatic brain-injury
- ubiquitin proteasome
- ubiquitin-proteasome system
- visual hallucinations
- Oxidative stress
- Biomarker
- ONSET PARKINSONISM
- Parkinson's disease
- UBIQUITIN-PROTEASOME SYSTEM
- VISUAL HALLUCINATIONS
- Ubiquitin proteasome
- mRNA splicing
- MITOCHONDRIAL DYSFUNCTION
- Alzheimer's disease
- OXIDATIVE STRESS
- Mitochondrial dysfunction
- LIPID-PEROXIDATION
- ALPHA-SYNUCLEIN
- DEPENDENT PROTEIN-DEGRADATION
- TRAUMATIC BRAIN-INJURY
- LEWY BODIES