Parkinson's disease (PD) is the second most common age related neurodegenerative disorder worldwide and presents as a progressive movement disorder. Globally seven million to 10 million people have Parkinson's disease. Parkinsonism is typically sporadic in nature. Loss of dopaminergic neurons from substantia nigra pars compacta (SNpc) and the neuronal intracellular Lewy body inclusions are the major cause of PD. Gene mutation and protein aggregation play a pivotal role in the degeneration of dopamine neurons. But the actual cause of dopamine degeneration remains unknown. However, several rare familial forms of PD are associated with genetic loci, and the recognition of causal mutations has provided insight into the disease process. Yet, the molecular pathways and gene transformation that trigger neuronal susceptibility are inadequately comprehended. The discovery of a mutation in new genes has provided a basis for much of the ongoing molecular work in the PD field and testing of targeted therapeutics. Single gene mutation in a dominantly or recessively inherited gene results a great impact in the development of Parkinson's disease. In this review, we summarize the molecular genetics of PD.
Parkinson disease (PD) is the most common chronic neurodegenerative disease that affects the brain, resulting in a progressive loss of coordination and movement to death and contributes to about 25-30% cases of dementia. An estimated seven million to 10million people worldwide have Parkinson's disease. It is characterized by the classical motor features of parkinsonism related to Lewy bodies and loss of dopaminergic neurons in the substantia nigra, and the major symptoms include problems with resting tremor, rigidity, bradykinesia, postural instability, speech dysfunction, psychiatric symptoms, sleep disorder and fatigue. Presently existing pharmacological and surgical treatments provides relief from a few motor symptoms, but do not halt the ultimate progression of the syndrome. The root cause of Parkinson's disease remains unknown. Although significant research advances illustrate distinct paths that closely try to disclose various mitochondrial, genetic, behavioral, environmental, and epigenetic causes that may lead to the development of PD. Most likely all study target the dysfunction of the ubiquitin-proteasome pathway, alpha-synuclein protein, PINK1 protein, PI3K/Akt/mTOR pathway. However, a better understanding of the disease is leading to new diagnostic tools and treatments.
Human immunodeficiency virus (HIV)-hepatitis C virus (HCV) coinfection is a major health problem around worldwide. One-third of the HIV-infected patients suffer from chronic hepatitis (HCV). The risk factors of coinfected patients are very high while compared to the monoinfected patients; they are having higher HCV viral load is associated with a severe liver damage. The use of highly active antiretroviral therapy (HAART) dramatically increases the survival of HIV/HCV-coinfected patients by preventing the depletion of CD4 cell counts and delaying the progression of fibrosis which reduces the complications related to end-stage liver damage. Reverse-transcriptase inhibitors and protease inhibitors are very commonly used drugs for the treatment of coinfection. Combination drugs and synthetic drugs are playing a pivotal role in the coinfection therapy. Under HAART, the coinfected patients are affected by many adverse effects such as mitochondrial toxicity, hypersensitivity, and lipodystrophy syndrome. However, the adverse effects of most herbal drugs are relatively less frequent when the drugs are used properly compared with synthetic drugs; it may help to protect the patients from severe adverse effects. This review collates to the importance of plant-derived drugs for the treatment of HIV-HCV coinfection.
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