Role of triggering receptor expressed on myeloid cells 2 (TREM2) in neurodegenerative dementias

Abstract

Dementia is a severe cognitive disability that interferes with the processes through which individuals interpret, encode, retrieve, and utilize data. Dementia prevalence increases dramatically in the late life, and currently, none of the treatments available can alter the underlying pathology after clinical onset. In 2010, about 35.6 million people worldwide were estimated to be affected by dementia, with these numbers estimated to double every two decades to hit 65.7 million in 2030 and 115.4 million in 2050 , respectively (Prince et al., 2013. Various neurodegenerative diseases (NDDs) including, Alzheimer's disease (AD), Parkinson's disease (PD), Lewy

Neurochemical Markers of Traumatic Brain Injury: Relevance to Acute Diagnostics, Disease Monitoring, and Neuropsychiatric Outcome Prediction

“…The shift between these two opposite functions is not well-understood. Triggering receptor expressed on myeloid cells 2 (TREM2) is a receptor mainly expressed on the surface of the microglia (63). Recently TREM2 has been found to play a role in the In Alzheimer's disease (AD).…”

TREM2 gene induces differentiation of induced pluripotent stem cells into dopaminergic neurons and promotes neuronal repair via TGF‐β activation in 6‐OHDA‐lesioned mouse model of Parkinson's disease

“…PD is a type of neurodegenerative disease, associated with degeneration of dopaminergic neurons 28 . Neurodegeneration is a debilitating condition which can result in nerve cell degeneration or death 34 . Overexpression of TREM2 has been reported to reduce dopaminergic neurodegeneration in the MPTP‐induced mouse model of PD 11 .…”

Neuroinflammation: A Potential Risk for Dementia

“…Mutations in microglia-related genes such as SOD1 (superoxide dismutase 1), C9Orf72 (ORF 72 on chromosome 9), TBK1 (TANK-binding kinase 1), OPTN (optineurin), SQSTM1 (Sequesterome-1), and VCP (Valosin-containing protein), which activate microgliaincrease the production of neurotoxic factor production, leading to neuroinflammation. Mutations in genes such as C9Orf72, PFN1 (Profilin), TREM2 and GRN (granulin) have been shown to lead to phagocytosis and associated degradation pathways that are regulated by microglial cells [ 105 ]. Further damage to motor neurons in ALS is caused by changes in these processes, leading to neurodegeneration, encouraging the progression of the disease [ 106 ].…”