MicroRNA a Potential Therapeutic Target for Alzheimer’s and Age-Related Macular Degeneration

MicroRNA a Potential Therapeutic Target for Alzheimer’s and Age-Related Macular Degeneration
Louisiana State University Health Sciences Center researchers in New Orleans have shown that TREM2, an innate immune receptor protein essential to the clearing of waste from the brain and retina, is diminished in age-related macular degeneration (AMD), identifying a key molecular pathway and possible therapeutic target. Loss of function of TREM2 has been associated with several pathogenic events in different progressive neurological diseases such as Alzheimer’s. The research paper, “microRNA-34a-Mediated Down-Regulation of the Microglial-Enriched Triggering Receptor and Phagocytosis-Sensor TREM2 in Age-Related Macular Degeneration,” was published in PLOS One. During the normal physiological processes, the brain and retina produce large quantities of waste products, such as amyloid protein, a hallmark of Alzheimer’s disease. This waste is cleared in a process that includes the TREM2 protein, localized in highly specialized cells called microglia which constitute the main form of active immune defense in the central nervous system (CNS). When the clearance system is not working properly, these waste products accumulate and lead to the formation of harmful structures, such as amyloid plaques. Mutations and loss of function of TREM2 have been linked to deficiencies in phagocytosis, the innate-immune system, axonal and synaptic abnormalities, and progressive dementia in several progressive neurodegenerative diseases of the CNS such as sporadic amyotrophic lateral sclerosis (ALS) and Alzheimer’s disease. Researchers studied the behavior of TREM2 in human retinal tissues affected by age-related mac
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