PAPER Chen L, Zhang J, Yang X, Wang S, Ye F
SEARCH RESULTS
340304 RESULTS
EMBO Workshop: Astrocytes 2025- From Molecules to Systems
CONFERENCE 2025-04-14 00:00:00-2025-04-18 00:00:00 Venice, Italy 14 – 18 April 2025 View Conference Website 0
PAPER Russell JK, Conley AC, Wilson JE, Newhouse PA
Cholinergic System Structure and Function Changes in Individuals with Down Syndrome During the Development of Alzheimer's Disease.
Curr Top Behav Neurosci. 2024 Nov 2; Epub 2024 Nov 2 PubMed.Trisomy 21
MUTATIONS APP Chromosome 21 Non-Coding Coding APP overexpression, possible modification of pathology/vulnerability by increased expression of other genes on chromosome 21. Neuropathology consistent with AD, usually developing by age 40 and often accompanied by CAA.
PAPER Jiang Y, Jiao B, Xiao X, Shen L
Genetics of frontotemporal dementia in China.
Amyotroph Lateral Scler Frontotemporal Degener. 2021 Aug;22(5-6):321-335. Epub 2021 Feb 4 PubMed.MAPT P301L
MUTATIONS MAPT 46010389 GRCh38/hg38 rs63751273 C T 44087755 GRCh37/hg19 rs63751273 C T g.123790C> T g.120969C> T Exon 10 Point, Missense Coding Strongly promotes β-sheet formation in 4R tau and accelerates the formation of paired helical filament. Decreases t
Amita Sehgal on New Role for Tau: Making Lipid Droplets in Glia?
COMMENT This very interesting finding describes a novel function for tau in the processing of peroxidated lipids from neurons. We previously showed that these lipids are transferred from neurons to glia in a daily sleep-dependent cycle, so this also indicates a r
Michael Irizarry, Akihiko Koyama, Taro Terauchi, Yukio Ishikawa on Lecanemab Bested Three Other Antibodies at Binding Soluble Aβ Aggregates
COMMENT This paper by Fertan et al. aligns with our understanding of the binding profile of lecanemab, an IgG1 antibody directed against aggregated soluble and insoluble forms of Aβ (U.S. Prescribing Information). In previous studies, lecanemab showed preferentia
Ruth Itzhaki on Can Heparin Delay Alzheimer’s Disease?
COMMENT It is surprising that no mention was made that not only APOE and tau, but also HSV1, along with diverse types of infectious pathogen—viruses, including SARS-COV-2, bacteria, and parasites—use HSPG for the first stage of attachment and entry into cells (Ak
Donald Weaver on Can Heparin Delay Alzheimer’s Disease?
COMMENT Heparin and heparan sulfate and are chemically related αβ-linked glycosaminoglycans (GAGs) composed of alternating sequences of glucosamine and uronic acid; the amino sugars may be N-acetylated or N-sulfated, with the latter being unique to these two poly
Róisín McManus on Some Plasma Proteins Bolster Phagocytosis and Metabolism in Microglia
COMMENT This new study by Lu and colleagues is an exciting new addition to the field of microglial signalling and regulation, particularly in how messengers from the blood can communicate with brain-resident immune cells. This paper builds on previous work from t
Per Hammarstrom on Amyloid Plaques Turn More Toxic as They Age
COMMENT This pioneering study by Hanrieder and co-workers aims to understand the initiation and progression of Aβ aggregate accumulation and correlations with CNS cell responses by spatial transcriptomics in the proximity of early and late Aβ aggregates. Chemical
Greg Lemke on A Match Made in Microglia? ApoE and Aβ Click in Lysosomes, Seeding Plaque
COMMENT Kaji and colleagues use a variety of experimental approaches to demonstrate that, in the AD brain, lipid-associated ApoE is phagocytically internalized into microglia together with lower-order polymers of Aβ, and that ApoE facilitates the dense fibrillar
Jason Ulrich on A Match Made in Microglia? ApoE and Aβ Click in Lysosomes, Seeding Plaque
COMMENT This is a fantastic study from the Simons lab that brings together a lot of key observations into an attractive theoretical framework for how APOE and microglia conspire to form nascent amyloid fibrils to seed pathology. It begs the question of whether de
Jessica Young on A Match Made in Microglia? ApoE and Aβ Click in Lysosomes, Seeding Plaque
COMMENT Genetics studies point to endo-lysosomal, immune, and lipid pathways as dysfunctional in AD, and many of these genes are highly expressed in glia. In this study, Kaji et al., perform an impressive amount of experiments to show microglial cells are necessa
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