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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Alzheimer Disease, Apolipoprotein E4, Brain, Case-Control Studies, Female, Gene Expression, Genetic Association Studies, Humans, Inflammation, Interleukin-4, Membrane Glycoproteins, Mutation, Missense, Myeloid Cells, Plaque, Amyloid, Receptors, Immunologic, Risk.
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Is the triggering receptor expressed on myeloid cells 2 ( TREM2 ) associated with enhanced inflammation , neuropathological lesions and increased risk for Alzheimer 's dementia? Context: The objective of this study was to elucidate the relationship between the triggering receptor expressed on myeloid cells 2 (TREM2) risk variant, neuropathological lesions, alterations in gene and protein expression, and the severity of neuroinflammation. The genetic association study of the R47 H TREM2 variant with Alzheimer's disease (AD), neuropathology, and changes in TREM2 and TYRO protein tyrosine kinase-binding protein (TYROBP) gene and protein expression, and neuroinflammatory markers. The TREM2 variant is associated with: (i) AD (odds ratio: 4.76; P = .014); (ii) increased density of amyloid plaques and neurofibrillary tangles in multiple brain regions; (iii) increased TREM2 (P = .041) and TYROBP (P = .006) gene expression; (iv) decreased TREM2 protein levels (P = .016); and (v) upregulation of proinflammatory cytokines (regulated on activation, normal T cell expressed and secreted [RANTES] and interferon [IFN] gamma) (P = .003) and nominal downregulation of protective markers (α2-macroglobulin, interleukin 4 or IL-4, and ApoA1) (P = .018).
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These findings link the TREM2 missense mutation with specific molecular abnormalities and increases in neuropathological lesions in the human brain. Final Decision: yes