PAPER Furukawa M, Shimoda H, Kajiwara T, Kato S, Yanagisawa S
SEARCH RESULTS
1268 RESULTS
Allan Butterfield on Aβ Dimers Block Glutamate Uptake, Fire Up Synapses
COMMENT This paper suggests that defects in GLT-1 (also known as EAAT2) in astrocytes lead to accumulation of synaptic glutamate, which causes hyperactivity, leading to excitotoxicity of and Ca2+ entry to neurons. Nearly two decades ago, our laboratory demonstrat
Wei Wang
Arlington, United States
Rik van der Kant on Familial AD Mutations, β-CTF, Spell Trouble for Endosomes
COMMENT This is a very impressive and exhaustive study by the Tessier-Lavigne lab showing that APP β-CTFs, but not Aβ, drives endosomal enlargement in human neurons from patients with familial AD (FAD). Using more than fifteen isogenic iPSC lines, the authors sho
Rick Livesey on Familial AD Mutations, β-CTF, Spell Trouble for Endosomes
COMMENT Pioneering work from several groups, most notably from Ralph Nixon and colleagues, identified dysfunction of the endolysosomal network in Alzheimer’s disease, and that this was due to abnormal processing of APP. This exciting study is an important contri
Christian Haass on Familial AD Mutations, β-CTF, Spell Trouble for Endosomes
COMMENT This paper reproduces findings in human iPSC-derived neurons that others made decades ago in much simpler cell systems. These cell lines are therefore a nice and important resource for future research, but I would have expected a balanced discussion and
Selina Wray, Charlie Arber on Familial AD Mutations, β-CTF, Spell Trouble for Endosomes
COMMENT Induced pluripotent stem cell (iPSC)-derived cell types are widely used as physiologically-relevant models of human neurodegenerative disease, but challenges still remain around the inherent variability driven largely by differing genetic backgrounds. A
Jessica Young on Familial AD Mutations, β-CTF, Spell Trouble for Endosomes
COMMENT Recent failures of Aβ-centric clinical trials highlight the need for investigating early cellular phenotypes that cause dysfunction upstream of amyloid and tau pathology in Alzheimer’s disease. Endosome enlargement is an early cytopathology in AD, and mul
Ralph Nixon on Familial AD Mutations, β-CTF, Spell Trouble for Endosomes
COMMENT This report on CRISPR-modified IPSC neurons expressing diverse APP and PSEN1 FAD mutations is a technical tour de force. It is a welcome confirmation of our previous findings on neurons in AD, FAD, and Down’s sydrome (DS) brains and human DS fibroblasts,
Familial AD Mutations, β-CTF, Spell Trouble for Endosomes
RESEARCH NEWS 2019-08-19 Research News Faltering endosomal trafficking appears to be the common modus operandi by a range of familial Alzheimer’s mutations. In the August 14 Neuron, researchers led by Marc Tessier-Lavigne of Stanford University reported initial findings from a pa
Amirhossein Feizi
Tehran, Iran, Islamic Republic of
PAPER Giorgi FS, Saccaro LF, Galgani A, Busceti CL, Biagioni F, Frati A, Fornai F
The role of Locus Coeruleus in neuroinflammation occurring in Alzheimer's disease.
Brain Res Bull. 2019 Nov;153:47-58. Epub 2019 Aug 13 PubMed: 31419539PAPER Crabbé M, Van der Perren A, Bollaerts I, Kounelis S, Baekelandt V, Bormans G, Casteels C, Moons L, Van Laere K
Increased P2X7 Receptor Binding Is Associated With Neuroinflammation in Acute but Not Chronic Rodent Models for Parkinson's Disease.
Front Neurosci. 2019;13:799. Epub 2019 Jul 31 PubMed: 31417352PAPER Takada-Takatori Y, Nakagawa S, Kimata R, Nao Y, Mizukawa Y, Urushidani T, Izumi Y, Akaike A, Tsuchida K, Kume T
Donepezil modulates amyloid precursor protein endocytosis and reduction by up-regulation of SNX33 expression in primary cortical neurons.
Sci Rep. 2019 Aug 15;9(1):11922. PubMed: 31417133PAPER Liu L, Lauro BM, Ding L, Rovere M, Wolfe MS, Selkoe DJ
Multiple BACE1 inhibitors abnormally increase the BACE1 protein level in neurons by prolonging its half-life.
Alzheimers Dement. 2019 Sep;15(9):1183-1194. Epub 2019 Aug 12 PubMed: 31416794Current Filters
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