Microglia TREM2R47H Alzheimer-linked variant enhances excitatory transmission and reduces LTP via increased TNF-α levels

Trem2 Splicing and Expression are Preserved in a Human Aβ-producing, Rat Knock-in Model of Trem2-R47H Alzheimer’s Risk Variant

(2020) Marc D. Tambini et al.   Scientific Reports

Opposite changes in APP processing and human Aβ levels in rats carrying either a protective or a pathogenic APP mutation

(2020) Marc D Tambini et al.   eLife

Tuning of glutamate, but not GABA, release by an intra-synaptic vesicles APP domain whose function can be modulated by β- or α-secretase cleavage

(2019) Wen Yao et al.   JOURNAL OF NEUROSCIENCE

Facilitation of glutamate, but not GABA , release in Familial Alzheimer's APP mutant Knock‐in rats with increased β‐cleavage of APP

(2019) Marc D. Tambini et al.   AGING CELL

The Microglial Innate Immune Receptor TREM2 Is Required for Synapse Elimination and Normal Brain Connectivity

(2018) Fabia Filipello et al.   IMMUNITY

Humanized TREM2 mice reveal microglia-intrinsic and -extrinsic effects of R47H polymorphism

(2018) Wilbur M. Song et al.   JOURNAL OF EXPERIMENTAL MEDICINE

TREM2 Is a Receptor for β-Amyloid that Mediates Microglial Function

(2018) Yingjun Zhao et al.   NEURON

Behavioral and transcriptomic analysis of Trem2-null mice: not all knockout mice are created equal

(2017) Silvia S Kang et al.   HUMAN MOLECULAR GENETICS

A Brief History of Long-Term Potentiation

(2017) Roger A. Nicoll   NEURON

TREM2 Binds to Apolipoproteins, Including APOE and CLU/APOJ, and Thereby Facilitates Uptake of Amyloid-Beta by Microglia

(2016) Felix L. Yeh et al.   NEURON

ADAM10 and BACE1 are localized to synaptic vesicles

(2015) Jolanta L. Lundgren et al.   JOURNAL OF NEUROCHEMISTRY

Presenilin-1 Knockin Mice Reveal Loss-of-Function Mechanism for Familial Alzheimer’s Disease

(2015) Dan Xia et al.   NEURON

Regulation of microglial survival and proliferation in health and diseases

(2015) Tyler K. Ulland et al.   SEMINARS IN IMMUNOLOGY

APP and APLP2 interact with the synaptic release machinery and facilitate transmitter release at hippocampal synapses

(2015) Tomas Fanutza et al.   eLife

Contribution of Alzheimer disease to mortality in the United States

(2014) B. D. James et al.   NEUROLOGY

APP Is Cleaved by Bace1 in Pre-Synaptic Vesicles and Establishes a Pre-Synaptic Interactome, via Its Intracellular Domain, with Molecular Complexes that Regulate Pre-Synaptic Vesicles Functions

(2014) Dolores Del Prete et al.   PLoS One

Presenilins regulate calcium homeostasis and presynaptic function via ryanodine receptors in hippocampal neurons

(2013) B. Wu et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

Interactome of the Amyloid Precursor Protein APP in Brain Reveals a Protein Network Involved in Synaptic Vesicle Turnover and a Close Association with Synaptotagmin-1

(2012) Bernhard M. Kohli et al.   JOURNAL OF PROTEOME RESEARCH

TREM2 Variants in Alzheimer's Disease

(2012) Rita Guerreiro et al.   NEW ENGLAND JOURNAL OF MEDICINE

Amyloid Precursor Protein Is Trafficked and Secreted via Synaptic Vesicles

(2011) Teja W. Groemer et al.   PLoS One

Identification of NEEP21 as a  -Amyloid Precursor Protein-Interacting Protein In Vivo That Modulates Amyloidogenic Processing In Vitro

(2010) E. M. Norstrom et al.   JOURNAL OF NEUROSCIENCE

Memory Deficits Due to Familial British Dementia BRI2 Mutation Are Caused by Loss of BRI2 Function Rather than Amyloidosis

(2010) R. Tamayev et al.   JOURNAL OF NEUROSCIENCE

Danish dementia mice suggest that loss of function and not the amyloid cascade causes synaptic plasticity and memory deficits

(2010) R. Tamayev et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

Maturation of BRI2 generates a specific inhibitor that reduces APP processing at the plasma membrane and in endocytic vesicles

(2009) Shuji Matsuda et al.   NEUROBIOLOGY OF AGING

BRI2 Inhibits Amyloid  -Peptide Precursor Protein Processing by Interfering with the Docking of Secretases to the Substrate

(2008) S. Matsuda et al.   JOURNAL OF NEUROSCIENCE