Can miRNAs Be Considered as Diagnostic and Therapeutic Molecules in Ischemic Stroke Pathogenesis?-Current Status.

Ischemic stroke is one of the leading causes of death worldwide. Clinical manifestations of stroke are long-lasting and causing economic burden on the patients and society. Current therapeutic modalities to treat ischemic stroke (IS) are unsatisfactory due to the intricate pathophysiology and poor functional recovery of brain cellular compartment. MicroRNAs (miRNA) are endogenously expressed small non-coding RNA molecules, which can act as translation inhibitors and play a pivotal role in the pathophysiology associated with IS. Moreover, miRNAs may be used as potential diagnostic and therapeutic tools in clinical practice; yet, the complete role of miRNAs is enigmatic during IS. In this review, we explored the role of miRNAs in the regulation of stroke risk factors viz., arterial hypertension, metabolic disorders, and atherosclerosis. Furthermore, the role of miRNAs were reviewed during IS pathogenesis accompanied by excitotoxicity, oxidative stress, inflammation, apoptosis, angiogenesis, neurogenesis, and Alzheimer's disease. The functional role of miRNAs is a double-edged sword effect in cerebral ischemia as they could modulate pathological mechanisms associated with risk factors of IS. miRNAs pertaining to IS pathogenesis could be potential biomarkers for stroke; they could help researchers to identify a particular stroke type and enable medical professionals to evaluate the severity of brain injury. Thus, ascertaining the role of miRNAs may be useful in deciphering their diagnostic role consequently it is plausible to envisage a suitable therapeutic modality against IS.

The role of microglia in the development of neurodegeneration.

Microglia-mediated central nervous system (CNS) inflammation is one of the key features of various neurodegenerative diseases, including Parkinson's and Alzheimer's diseases. In the last few years, a number of studies have investigated the link between neurodegenerative diseases and CNS glial cells, in particular microglia. Microglial cells are the main resident immune cells and comprise approximately 10-15% of all CNS cells. Microglia at rest regulates CNS homeostasis via phagocytic activity, by removing pathogens and cell detritus. "Resting" microglia cells transform into an activated form and produce inflammatory mediators, thus protecting neurons and providing defense against invading pathogens. Excessive inflammation leads to neuronal damage and neurodegenerative diseases. Various microglial reactions at different stages of the disease can open up new directions for treatment interventions and modification of the inflammatory activity. This review focuses on the potential role of microglia and the dynamic M1/M2 phenotype changes that are critically linked to certain neurodegenerative diseases.