TREM2 deficiency attenuates neuroinflammation and protects against neurodegeneration in a mouse model of tauopathy

Significance Alzheimer’s disease (AD) is the most common cause of dementia and is a major public health problem for which there is currently no disease-modifying treatment. There is an urgent need for greater understanding of the molecular mechanisms underlying neurodegeneration in patients to create better therapeutic options. Recently, genetic studies uncovered novel AD risk variants in the microglial receptor, triggering receptor expressed on myeloid cells 2 (TREM2). Previous studies suggested that loss of TREM2 function worsens amyloid-β (Aβ) plaque-related toxicity. In contrast, we observe TREM2 deficiency mitigates neuroinflammation and protects against brain atrophy in the context of tau pathology. These findings indicate dual roles for TREM2 and microglia in the context of amyloid versus tau pathology, which are important to consider for potential treatments targeting TREM2.</jats:p

Jet properties from π±\pi^{\pm} - h±h^{\pm} correlation in p+pp+p and dd+Au collisions at sNN\sqrt{s_{NN}} = 200 GeV

We review recent results on the charged pion - charged hadron correlation in $p+p$ and $d$ + Au collisions as measured by the PHENIX Collaboration. Properties of di-jet system, such as the jet shape, associated hadron yield per trigger pion, and the underlying event are extracted statistically from the $\pi^{\pm}-h^{\pm}$ correlation function in $\Delta\phi$ and $\Delta\eta$. For jet triggered with high $p_T$ pions ($p_T>5$ GeV/c), no apparent differences in the jet properties are seen between $p+p$ and $d$ + Au.Comment: Proceeding for Correlation and Fluctuation Workshop at MIT (April 2005), 11 pages, 17 figures, update a couple of formula