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Showing 1-18 of 18 results for "SML1954" within Papers
Andy P Tsai et al.
Neurobiology of disease, 153, 105303-105303 (2021-02-26)
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline, robust microgliosis, neuroinflammation, and neuronal loss. Genome-wide association studies recently highlighted a prominent role for microglia in late-onset AD (LOAD). Specifically, inositol polyphosphate-5-phosphatase (INPP5D), also known as SHIP1
Teemu Natunen et al.
Molecular neurodegeneration, 15(1), 66-66 (2020-11-11)
Alzheimer's disease (AD) is the most common neurodegenerative disease and type 2 diabetes (T2D) plays an important role in conferring the risk for AD. Although AD and T2D share common features, the common molecular mechanisms underlying these two diseases remain
Substrate-targeting ?-secretase modulators
Kukar TL
Nature, 453, 925-929 (2008)
Chantal M Ferguson et al.
Alzheimer's & dementia : the journal of the Alzheimer's Association, 20(4), 2632-2652 (2024-02-20)
The most significant genetic risk factor for late-onset Alzheimer's disease (AD) is APOE4, with evidence for gain- and loss-of-function mechanisms. A clinical need remains for therapeutically relevant tools that potently modulate APOE expression. We optimized small interfering RNAs (di-siRNA, GalNAc)
Marcus Bäck et al.
Chemistry (Weinheim an der Bergstrasse, Germany), 22(51), 18335-18338 (2016-11-04)
Deposits comprised of amyloid-β (Aβ) are one of the pathological hallmarks of Alzheimer's disease (AD) and small hydrophobic ligands targeting these aggregated species are used clinically for the diagnosis of AD. Herein, we observed that anionic oligothiophenes efficiently displaced X-34
Sangderk Lee et al.
Cell reports, 42(3), 112196-112196 (2023-03-06)
The E4 allele of Apolipoprotein E (APOE) is associated with both metabolic dysfunction and a heightened pro-inflammatory response: two findings that may be intrinsically linked through the concept of immunometabolism. Here, we combined bulk, single-cell, and spatial transcriptomics with cell-specific
Akshay Kapadia et al.
Autophagy, 20(1), 166-187 (2023-08-29)
AD: Alzheimer disease; APP: amyloid beta precursor protein; ATG: autophagy related; Aβ: amyloid-β; CTSD: cathepsin D; DAPI: 4',6-diamidino-2-phenylindole; EEA1: early endosome antigen 1; FA: formic acid; GFP: green fluorescent protein; LAMP2: lysosomal-associated membrane protein 2; MAP1LC3/LC3: microtubule-associated protein 1 light
Lina Vandermeulen et al.
Molecular neurodegeneration, 19(1), 37-37 (2024-04-24)
Microglia play important roles in maintaining brain homeostasis and neurodegeneration. The discovery of genetic variants in genes predominately or exclusively expressed in myeloid cells, such as Apolipoprotein E (APOE) and triggering receptor expressed on myeloid cells 2 (TREM2), as the
Andy P Tsai et al.
Immunity, 56(9), 2121-2136 (2023-09-03)
Genetic association studies have demonstrated the critical involvement of the microglial immune response in Alzheimer's disease (AD) pathogenesis. Phospholipase C-gamma-2 (PLCG2) is selectively expressed by microglia and functions in many immune receptor signaling pathways. In AD, PLCG2 is induced uniquely
Visualization of fibrillar amyloid deposits in living, transgenic Caenorhabditis elegans animals using the sensitive amyloid dye, X-34
Link CD
Neurobiology of Aging, 22, 217-226 (2001)
Tae-Kyung Kim et al.
Experimental & molecular medicine, 54(12), 2148-2161 (2022-12-07)
The clinical progression of neurodegenerative diseases correlates with the spread of proteinopathy in the brain. The current understanding of the mechanism of proteinopathy spread is far from complete. Here, we propose that inflammation is fundamental to proteinopathy spread. A sequence
Heidi Olzscha et al.
Cell chemical biology, 24(1), 9-23 (2016-12-19)
Lysine acetylation is becoming increasingly recognized as a general biological principle in cellular homeostasis, and is subject to abnormal control in different human pathologies. Here, we describe a global effect on amyloid-like protein aggregation in human cells that results from
Monica Xiong et al.
Science translational medicine, 13(581) (2021-02-19)
The ε4 allele of the apolipoprotein E (APOE) gene is the strongest genetic risk factor for late-onset Alzheimer's disease (AD) and greatly influences the development of amyloid-β (Aβ) pathology. Our current study investigated the potential therapeutic effects of the anti-human
Taweesak Tangrodchanapong et al.
Molecules (Basel, Switzerland), 26(8) (2021-05-01)
The pathological finding of amyloid-β (Aβ) aggregates is thought to be a leading cause of untreated Alzheimer's disease (AD). In this study, we isolated 2-butoxytetrahydrofuran (2-BTHF), a small cyclic ether, from Holothuria scabra and demonstrated its therapeutic potential against AD
Annerieke Sierksma et al.
EMBO molecular medicine, 12(3), e10606-e10606 (2020-01-18)
Polygenic risk scores have identified that genetic variants without genome-wide significance still add to the genetic risk of developing Alzheimer's disease (AD). Whether and how subthreshold risk loci translate into relevant disease pathways is unknown. We investigate here the involvement
Megan E Bosch et al.
Molecular neurodegeneration, 19(1), 18-18 (2024-02-17)
It has recently become well-established that there is a connection between Alzheimer's disease pathology and gut microbiome dysbiosis. We have previously demonstrated that antibiotic-mediated gut microbiota perturbations lead to attenuation of Aβ deposition, phosphorylated tau accumulation, and disease-associated glial cell
Insup Choi et al.
Nature cell biology, 25(7), 963-974 (2023-05-26)
Dysfunctional autophagy has been implicated in the pathogenesis of Alzheimer's disease (AD). Previous evidence suggested disruptions of multiple stages of the autophagy-lysosomal pathway in affected neurons. However, whether and how deregulated autophagy in microglia, a cell type with an important
S D Styren et al.
The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society, 48(9), 1223-1232 (2000-08-19)
X-34, a lipophilic, highly fluorescent derivative of Congo red, was examined as a histochemical stain for pathological changes in Alzheimer's disease (AD). X-34 intensely stained neuritic and diffuse plaques, neurofibrillary tangles (NFTs), neuropil threads, and cerebrovascular amyloid. Comparison to standard
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