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Showing 1-30 of 47 results for "MABN10" within Papers
Eitan Wong et al.
Proceedings of the National Academy of Sciences of the United States of America, 116(13), 6385-6390 (2019-03-10)
The mechanism by which γ-secretase activating protein (GSAP) regulates γ-secretase activity has not yet been elucidated. Here, we show that knockout of GSAP in cultured cells directly reduces γ-secretase activity for Aβ production, but not for Notch1 cleavage, suggesting that
Rémi Opsomer et al.
eNeuro, 7(3) (2020-04-25)
The amyloid precursor protein (APP) has been extensively studied as the precursor of the β-amyloid (Aβ) peptide, the major component of the senile plaques found in the brain of Alzheimer's disease (AD) patients. However, the function of APP per se
Cheril Tapia-Rojas et al.
Journal of neurochemistry, 144(4), 443-465 (2017-12-15)
Alzheimer's disease (AD) is a neurodegenerative pathology characterized by aggregates of amyloid-β (Aβ) and phosphorylated tau protein, synaptic dysfunction, and spatial memory impairment. The Wnt signaling pathway has several key functions in the adult brain and has been associated with
Henna Jäntti et al.
Journal of neuroinflammation, 19(1), 147-147 (2022-06-16)
Microglia are the endogenous immune cells of the brain and act as sensors of pathology to maintain brain homeostasis and eliminate potential threats. In Alzheimer's disease (AD), toxic amyloid beta (Aβ) accumulates in the brain and forms stiff plaques. In
Luisa Diomede et al.
Neurobiology of disease, 62, 521-532 (2013-11-05)
Although Alzheimer's disease (AD) is usually sporadic, in a small proportion of cases it is familial and can be linked to mutations in β-amyloid precursor protein (APP). Unlike the other genetic defects, the mutation [alanine-673→valine-673] (A673V) causes the disease only
Isaak Beyer et al.
Chemistry (Weinheim an der Bergstrasse, Germany), 22(25), 8685-8693 (2016-05-12)
In addition to the prototypic amyloid-β (Aβ) peptides Aβ1-40 and Aβ1-42 , several Aβ variants differing in their amino and carboxy termini have been described. Synthetic availability of an Aβ variant is often the key to study its role under
Dingding Mo et al.
Cells, 9(10) (2020-10-03)
Alzheimer's disease (AD) is an age-related detrimental dementia. Amyloid beta peptides (Aβ) play a crucial role in the pathology of AD. In familial AD, Aβ are generated from the full-length amyloid beta precursor protein (APP) via dysregulated proteolytic processing; however
Lou Fourriere et al.
Traffic (Copenhagen, Denmark), 23(3), 158-173 (2022-01-26)
The intracellular trafficking of β-site amyloid precursor protein (APP) cleaving enzyme (BACE1) and APP regulates amyloid-β production. Our previous work demonstrated that newly synthesized BACE1 and APP are segregated into distinct trafficking pathways from the trans-Golgi network (TGN), and that
Jordan H Cater et al.
Cells, 11(7) (2022-04-13)
Plasminogen activator inhibitor type-2 (PAI-2), a member of the serpin family, is dramatically upregulated during pregnancy and in response to inflammation. Although PAI-2 exists in glycosylated and non-glycosylated forms in vivo, the majority of in vitro studies of PAI-2 have
Larisa Chernyaeva et al.
EMBO reports, 24(7), e56467-e56467 (2023-05-08)
The APOE4 variant of apolipoprotein E (apoE) is the most prevalent genetic risk allele associated with late-onset Alzheimer's disease (AD). ApoE interacts with complement regulator factor H (FH), but the role of this interaction in AD pathogenesis is unknown. Here
Mahfuz B Khan et al.
Journal of neurovirology, 22(2), 179-190 (2015-09-27)
In the era of combined antiretroviral therapy (CART), many of the complications due to HIV-1 infection have diminished. One exception is HIV-associated neurocognitive disorder (HAND). HAND is a spectrum of disorders in cognitive function that ranges from asymptomatic disease to
Lina M Vargas et al.
PloS one, 9(3), e92309-e92309 (2014-03-25)
The early stages of Alzheimer's disease are characterised by impaired synaptic plasticity and synapse loss. Here, we show that amyloid-β oligomers (AβOs) activate the c-Abl kinase in dendritic spines of cultured hippocampal neurons and that c-Abl kinase activity is required
Yifei Zhong et al.
Journal of neurochemistry, 150(1), 74-87 (2019-05-12)
Soluble oligomers of the 42-amino acid amyloid beta (Aβ42) peptide are highly toxic and suspected as the causative agent of synaptic dysfunction and neuronal loss in Alzheimer's disease (AD). Previously, we have shown that a small, D-amino acid Aβ42-oligomer interacting
Tomas T Roos et al.
Acta neuropathologica, 142(4), 669-687 (2021-07-18)
The amyloid-beta peptide (Aβ) is thought to have prion-like properties promoting its spread throughout the brain in Alzheimer's disease (AD). However, the cellular mechanism(s) of this spread remains unclear. Here, we show an important role of intracellular Aβ in its
Baiba Jansone et al.
Pharmacological research, 113(Pt B), 781-787 (2016-06-28)
The prevalence of Alzheimer's disease (AD) is higher in females than in males, and causes more severe cognitive, memory and behavioral impairments. Previously, in male transgenic (Tg) APPSweDI mice, we reported that the novel lipophilic 1,4-dihydropyridine (DHP) derivative AP-12 crossed
Liping Li et al.
Human molecular genetics, 29(11), 1833-1852 (2020-01-17)
Abnormal modification of 5-hydroxymethylcytosine (5hmC) is closely related to the occurrence of Alzheimer's disease (AD). However, the role of 5hmC and its writers, ten-eleven translocation (Tet) proteins, in regulating the pathogenesis of AD remains largely unknown. We detected a significant
Deficits in the miRNA-34a-regulated endogenous TREM2 phagocytosis sensor-receptor in Alzheimer's disease (AD); an update.
Bhattacharjee, S; Zhao, Y; Lukiw, WJ
Frontiers in Aging Neuroscience null
Alicia González Díaz et al.
ACS chemical neuroscience, 15(14), 2586-2599 (2024-07-09)
Aβ oligomers are being investigated as cytotoxic agents in Alzheimer's disease (AD). Because of their transient nature and conformational heterogeneity, the relationship between the structure and activity of these oligomers is still poorly understood. Hence, methods for stabilizing Aβ oligomeric
Jens V Andersen et al.
Neurobiology of disease, 148, 105198-105198 (2020-11-27)
Alzheimer's disease (AD) leads to cerebral accumulation of insoluble amyloid-β plaques causing synaptic dysfunction and neuronal death. Neurons rely on astrocyte-derived glutamine for replenishment of the amino acid neurotransmitter pools. Perturbations of astrocyte glutamine synthesis have been described in AD
Irina Belaya et al.
International journal of molecular sciences, 22(16) (2021-08-28)
Dysregulation of brain iron metabolism is one of the pathological features of aging and Alzheimer's disease (AD), a neurodegenerative disease characterized by progressive memory loss and cognitive impairment. While physical inactivity is one of the risk factors for AD and
Lulu Jiang et al.
Frontiers in neuroscience, 18, 1372297-1372297 (2024-04-04)
The study of the pathophysiology study of Alzheimer's disease (AD) has been hampered by lack animal models that recapitulate the major AD pathologies, including extracellular -amyloid (A) deposition, intracellular aggregation of microtubule associated protein tau (MAPT), inflammation and neurodegeneration. The
Surjyadipta Bhattacharjee et al.
PloS one, 11(3), e0150211-e0150211 (2016-03-08)
The aggregation of Aβ42-peptides and the formation of drusen in age-related macular degeneration (AMD) are due in part to the inability of homeostatic phagocytic mechanisms to clear self-aggregating Aβ42-peptides from the extracellular space. The triggering receptor expressed in myeloid/microglial cells-2
Johnny Habchi et al.
Science advances, 2(2), e1501244-e1501244 (2016-03-05)
The conversion of the β-amyloid (Aβ) peptide into pathogenic aggregates is linked to the onset and progression of Alzheimer's disease. Although this observation has prompted an extensive search for therapeutic agents to modulate the concentration of Aβ or inhibit its
Wei Hong Toh et al.
Traffic (Copenhagen, Denmark), 18(3), 159-175 (2016-12-22)
The intracellular trafficking and proteolytic processing of the membrane-bound amyloid precursor protein (APP) are coordinated events leading to the generation of pathogenic amyloid-beta (Aβ) peptides. The membrane transport of newly synthesized APP from the Golgi to the endolysosomal system is
Daniela A Gutierrez et al.
Frontiers in cellular neuroscience, 13, 526-526 (2019-12-19)
Spine pathology has been implicated in the early onset of Alzheimer's disease (AD), where Aβ-Oligomers (AβOs) cause synaptic dysfunction and loss. Previously, we described that pharmacological inhibition of c-Abl prevents AβOs-induced synaptic alterations. Hence, this kinase seems to be a
Janaina Balthazar et al.
Frontiers in aging neuroscience, 10, 288-288 (2018-10-16)
Alzheimer's disease (AD) is associated with a progressive dementia, and there is good evidence that it is more pronounced in individuals that have fewer stimuli during their lives. Environmental stimulation promotes morphological and functional changes in the brain, leading to
Kirk M Brown et al.
Nature biotechnology, 40(10), 1500-1508 (2022-06-03)
Therapeutics based on short interfering RNAs (siRNAs) delivered to hepatocytes have been approved, but new delivery solutions are needed to target additional organs. Here we show that conjugation of 2'-O-hexadecyl (C16) to siRNAs enables safe, potent and durable silencing in
Jens V Andersen et al.
Cell death & disease, 12(11), 954-954 (2021-10-18)
Alzheimer's disease (AD) is an unremitting neurodegenerative disorder characterized by cerebral amyloid-β (Aβ) accumulation and gradual decline in cognitive function. Changes in brain energy metabolism arise in the preclinical phase of AD, suggesting an important metabolic component of early AD
Cheril Tapia-Rojas et al.
Molecular neurodegeneration, 10, 62-62 (2015-11-23)
L-methionine, the principal sulfur-containing amino acid in proteins, plays critical roles in cell physiology as an antioxidant and in the breakdown of fats and heavy metals. Previous studies suggesting the use of L-methionine as a treatment for depression and other
Céline Vrancx et al.
Molecular neurobiology, 58(12), 6647-6669 (2021-10-06)
The β-amyloid peptide (Aβ) is found as amyloid fibrils in senile plaques, a typical hallmark of Alzheimer's disease (AD). However, intermediate soluble oligomers of Aβ are now recognized as initiators of the pathogenic cascade leading to AD. Studies using recombinant
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