Results 1 to 10 of about 22,048 (146)
Presenilin L166P Mutation, a Model of Familial Alzheimer's Disease, Leads to Early Onset Bone Loss. [PDF]
Compr PhysiolFemale‐specific bone loss in Alzheimer's disease mouse models: There is a significant alteration of bone phenotype during Alzheimer's disease. Using integrated imaging and biological assays, we observed changes in the bone microarchitecture, composition, and function in PSEN K1 and PSEN1/hAPP Tg+ mice, predominantly in the females. ABSTRACT Accelerated
Suryadevara V +12 more
europepmc +2 more sources
Presenilin-mediated cleavage of APP regulates synaptotagmin-7 and presynaptic plasticity
Nature Communications, 2018 Mutations in presenilin, which cleaves amyloid precursor protein, cause familial Alzheimer’s Disease. Here, the authors show that loss of presenilin leads to loss of synaptotagmin 7, leading to impaired presynaptic release.
Gaël Barthet +2 more
exaly +2 more sources
Frontiers in Pharmacology, 2022 Although dysautonomia was documented in inflammatory bowel disease, with activation of the stress-related sympathetic system, the role of agonists/antagonists of the adrenergic receptors is not conclusive. Moreover, ulcerative colitis was recently linked
Salma Nasser +4 more
doaj +1 more source
Frontiers in Aging Neuroscience, 2022 Alzheimer’s disease (AD), a neurodegenerative disorder that can occur in middle or old age, is characterized by memory loss, a continuous decline in thinking, behavioral and social skills that affect the ability of an individual to function independently.
Gustavo Lopez-Toledo +6 more
doaj +1 more source
Intracellular calcium deficits in Drosophila cholinergic neurons expressing wild type or FAD-mutant presenilin. [PDF]
PLoS ONE, 2009 Much of our current understanding about neurodegenerative diseases can be attributed to the study of inherited forms of these disorders. For example, mutations in the presenilin 1 and 2 genes have been linked to early onset familial forms of Alzheimer's ...
Kinga Michno +4 more
doaj +1 more source
Frontiers in Aging Neuroscience, 2022 The amyloid hypothesis for the pathogenesis of Alzheimer’s disease (AD) is widely accepted. Last year, the US Food and Drug Administration considered amyloid-β peptide (Aβ) as a surrogate biomarker and approved an anti-Aβ antibody, aducanumab, although ...
Shigeki Kawabata
doaj +1 more source
eLife, 2022 Cleavage of membrane proteins in the lipid bilayer by intramembrane proteases is crucial for health and disease. Although different lipid environments can potently modulate their activity, how this is linked to their structural dynamics is unclear. Here,
Lukas P Feilen +5 more
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Human PSEN1 Mutant Glia Improve Spatial Learning and Memory in Aged Mice
Cells, 2022 The PSEN1 ΔE9 mutation causes a familial form of Alzheimer’s disease (AD) by shifting the processing of amyloid precursor protein (APP) towards the generation of highly amyloidogenic Aβ42 peptide.
Henna Jäntti +18 more
doaj +1 more source
Frontiers in Genetics, 2023 Heparan sulfate modified proteins or proteoglycans (HSPGs) are an abundant class of cell surface and extracellular matrix molecules. They serve important co-receptor functions in the regulation of signaling as well as membrane trafficking.
Nicholas Schultheis +8 more
doaj +1 more source
The Amyloid Cascade Hypothesis in Alzheimer’s Disease: Should We Change Our Thinking?
Biomolecules, 2023 Old age increases the risk of Alzheimer’s disease (AD), the most common neurodegenerative disease, a devastating disorder of the human mind and the leading cause of dementia.
Markku Kurkinen +5 more
doaj +1 more source