32 RESULTS
COMMENT The actions of TREM2 are extraordinarily complicated and not easily understood, at least so far. Some of the essential issues have been confounded by the complexity of the science, the use of a narrow range of disease endpoints, and the use of only a few
COMMENT In this exciting new study, Wyss-Coray and colleagues report novel CNS actions of CD22, a well-studied B cell SIGLEC whose best-documented actions are to inhibit B cell receptor signaling. They originally identified CD22 in a screen for modifiers of micro
COMMENT Huang et al. report, in an elegant and detailed study, the central roles played by the TAM receptors Axl and Mer in amyloidogenic models of AD. There are a few surprises that will provoke re-evaluation of exactly how microglia act to actively influence th
COMMENT This an impressive and important paper. Key to this study is the development of the HAE-4 anti-ApoE antibody and its specificity for poorly lipidated forms of ApoE, which are preferentially incorporated into amyloid plaques. The study is the quintessentia
COMMENT Andreone and colleagues have provided an extensive and compelling study on the roles of the PLCγ2 in human iPSC-derived microglia-like cells. A significant outcome of this study is the validation that the findings in the human iMG cells largely recapitula
COMMENT The roles of TREM2 in AD pathogenesis have commanded substantial attention following from the recognition that TREM2 variants are associated with dramatically elevated AD risk. Previous work from this group reported that soluble forms of TREM2 were found
COMMENT New work from the Wyss-Coray lab reports that CD22 plays a role in regulating the phagocytic capacity of microglia. This is a compelling paper that adds depth to our understanding of the intricate mechanisms that act to regulate microglial actions. CD22 i
COMMENT Zhong and colleagues have recently reported a remarkable series of findings that demonstrate that soluble forms of TREM2 exhibit cell-autonomous actions and act to mitigate AD pathogenesis in mouse models of AD. These observations serve to focus attention
COMMENT Pan et al. report that oral administration of the flavonoid rutin to mouse models of Alzheimer’s disease results in amelioration of cognition deficits as well as a broad array of AD-related phenotypes. They report a dramatic reduction in plaque burden, an
COMMENT The congressional support for AD research in the recent past is extraordinary, and it is reassuring that our elected representatives have come to recognize the magnitude of the impact of the disease and provide new resources for research. The level of fun
COMMENT Liao et al. have reported that antibodies directed at human ApoE isoforms can reduce amyloid plaque burden in a mouse model of AD expressing human ApoE4. This study, like its predecessors from the Holtzman lab, derives from the recognition that plaques in
COMMENT The paper by Zhao and colleagues reports that Trem2 is a receptor for Aβ, joining a long list of cell surface Aβ-binding proteins on microglia. The authors argue that Trem2 preferentially interacts with Aβ oligomers, with Kd’s in the nM range. A point of
COMMENT The authors present an intriguing study that highlights the interplay between microglia and neurons in the progression of amyloid pathology in a mouse model of Alzheimer’s disease. Although others have demonstrated that early intervention with CSF1R inhib
COMMENT There is now a substantial literature documenting the linkage of immune cell genes to neurodegenerative disease. This study validates the conclusion that microglia (and other myeloid subpopulations) contribute to risk for late-onset AD. Sims et al. have i
COMMENT Zhong et al. report that soluble forms of TREM2 are able to elicit a robust proinflammatory response and promote survival in primary microglia. These findings provide a completely novel take on the biological roles of soluble TREM2. Previous work has show
