[PDF][PDF] The TREM2-APOE pathway drives the transcriptional phenotype of dysfunctional microglia in neurodegenerative diseases
…, E Tjon, F Mazaheri, K Hartmann, A Madi, JD Ulrich… - Immunity, 2017 - cell.com
Microglia play a pivotal role in the maintenance of brain homeostasis but lose homeostatic
function during neurodegenerative disorders. We identified a specific apolipoprotein E (APOE)…
function during neurodegenerative disorders. We identified a specific apolipoprotein E (APOE)…
[HTML][HTML] TREM2 lipid sensing sustains the microglial response in an Alzheimer's disease model
Triggering receptor expressed on myeloid cells 2 (TREM2) is a microglial surface receptor
that triggers intracellular protein tyrosine phosphorylation. Recent genome-wide association …
that triggers intracellular protein tyrosine phosphorylation. Recent genome-wide association …
[PDF][PDF] TREM2 maintains microglial metabolic fitness in Alzheimer's disease
Elevated risk of developing Alzheimer's disease (AD) is associated with hypomorphic variants
of TREM2, a surface receptor required for microglial responses to neurodegeneration, …
of TREM2, a surface receptor required for microglial responses to neurodegeneration, …
Microglia-mediated T cell infiltration drives neurodegeneration in tauopathy
Extracellular deposition of amyloid-β as neuritic plaques and intracellular accumulation of
hyperphosphorylated, aggregated tau as neurofibrillary tangles are two of the characteristic …
hyperphosphorylated, aggregated tau as neurofibrillary tangles are two of the characteristic …
Human and mouse single-nucleus transcriptomics reveal TREM2-dependent and TREM2-independent cellular responses in Alzheimer's disease
…, JA Schneider, MR Nichols, SA Beausoleil, JD Ulrich… - Nature medicine, 2020 - nature.com
Glia have been implicated in Alzheimer’s disease (AD) pathogenesis. Variants of the microglia
receptor triggering receptor expressed on myeloid cells 2 (TREM2) increase AD risk, and …
receptor triggering receptor expressed on myeloid cells 2 (TREM2) increase AD risk, and …
TREM2-mediated early microglial response limits diffusion and toxicity of amyloid plaques
Triggering receptor expressed on myeloid cells 2 (TREM2) is a microglial receptor that
recognizes changes in the lipid microenvironment, which may occur during amyloid β (Aβ) …
recognizes changes in the lipid microenvironment, which may occur during amyloid β (Aβ) …
ApoE isoform–and microbiota-dependent progression of neurodegeneration in a mouse model of tauopathy
Tau-mediated neurodegeneration is a hallmark of Alzheimer’s disease. Primary tauopathies
are characterized by pathological tau accumulation and neuronal and synaptic loss. …
are characterized by pathological tau accumulation and neuronal and synaptic loss. …
[PDF][PDF] Selective removal of astrocytic APOE4 strongly protects against tau-mediated neurodegeneration and decreases synaptic phagocytosis by microglia
The apolipoprotein E (APOE) gene is the strongest genetic risk factor for Alzheimer's disease
and directly influences tauopathy and tau-mediated neurodegeneration. ApoE4 has strong …
and directly influences tauopathy and tau-mediated neurodegeneration. ApoE4 has strong …
TREM2 deficiency attenuates neuroinflammation and protects against neurodegeneration in a mouse model of tauopathy
CEG Leyns, JD Ulrich, MB Finn… - Proceedings of the …, 2017 - National Acad Sciences
Variants in the gene encoding the triggering receptor expressed on myeloid cells 2 (TREM2)
were recently found to increase the risk for developing Alzheimer’s disease (AD). In the …
were recently found to increase the risk for developing Alzheimer’s disease (AD). In the …
[HTML][HTML] Altered microglial response to Aβ plaques in APPPS1-21 mice heterozygous for TREM2
JD Ulrich, MB Finn, Y Wang, A Shen, TE Mahan… - Molecular …, 2014 - Springer
Background Recent genome-wide association studies linked variants in TREM2 to a strong
increase in the odds of developing Alzheimer’s disease. The mechanism by which TREM2 …
increase in the odds of developing Alzheimer’s disease. The mechanism by which TREM2 …