Results 41 to 50 of about 365,500 (282)

Amyloid beta and diabetic pathology cooperatively stimulate cytokine expression in an Alzheimer's mouse model [PDF]

open access: yes, 2020
Background Diabetes is a risk factor for developing Alzheimer's disease (AD); however, the mechanism by which diabetes can promote AD pathology remains unknown.
Fernández Ponce, Cecilia Matilde   +7 more
core   +3 more sources

Decoding Conformational Imprint of Convoluted Molecular Interactions Between Prenylflavonoids and Aggregated Amyloid-Beta42 Peptide Causing Alzheimer’s Disease

open access: yesFrontiers in Chemistry, 2021
Protein misfolding occurs due to the loss of native protein structure and adopts an abnormal structure, wherein the misfolded proteins accumulate and form aggregates, which result in the formation of amyloid fibrils that are associated with ...
E. Srinivasan   +8 more
doaj   +1 more source

Membrane biophysics and mechanics in Alzheimer's disease [PDF]

open access: yes, 2010
Alzheimer's disease is a chronic neurodegenerative disorder characterized by neuronal loss, cerebrovascular inflammation, and accumulation of senile plaques in the brain parenchyma and cerebral blood vessels. Amyloid-β peptide (Aβ), a major component
Askarova, Sholpan   +2 more
core   +1 more source

Lipofuscin Hypothesis of Alzheimer’s Disease

open access: yesDementia and Geriatric Cognitive Disorders Extra, 2011
The primary culprit responsible for Alzheimer’s disease (AD) remains unknown. Aβ protein has been identified as the main component of amyloid of senile plaques, the hallmark lesion of AD, but it is not definitively established whether the formation of ...
Giorgio Giaccone   +3 more
doaj   +1 more source

Berberine Reduces Aβ42 Deposition and Tau Hyperphosphorylation via Ameliorating Endoplasmic Reticulum Stress

open access: yesFrontiers in Pharmacology, 2021
Alzheimer’s disease (AD) is tightly related to endoplasmic reticulum stress (ER stress), which aggravates two dominant pathological manifestations of AD: senile plaques and neurofibrillary tangles. Berberine is widely applied in the clinical treatment of
Yue Wu   +6 more
doaj   +1 more source

HEWL interacts with dissipated oleic acid micelles, and decreases oleic acid cytotoxicity.

open access: yesPLoS ONE, 2019
Senile plaques are well-known hallmarks of Alzheimer's Diseases (AD). However, drugs targeting tangles of the protein tau and plaques of β-amyloid have no significant effect on disease progression, and the studies on the underlying mechanism of AD remain
Qin Huang   +5 more
doaj   +1 more source

Beyond Cholinesterase Inhibition. Anti-Inflammatory Role and Pharmacological Profile of Current Drug Therapy for Alzheimer's Disease [PDF]

open access: yes, 2016
Inflammation is a common response of an individual against either exogenous or endogenous damage. The role of inflammation and of inflammatory cells recently emerged also in the pathogenesis of neurodegenerative disorders. Experimental evidences show how
GIUBILEI, Franco
core   +1 more source

Amyloid-β Peptide Impact on Synaptic Function and Neuroepigenetic Gene Control Reveal New Therapeutic Strategies for Alzheimer’s Disease

open access: yesFrontiers in Molecular Neuroscience, 2020
Amyloid-β (Aβ) peptides can form protease-resistant aggregates within and outside of neurons. Accumulation of these aggregates is a hallmark of Alzheimer’s disease (AD) neuropathology and contributes to devastating cognitive deficits associated with this
Bhanu Chandra Karisetty   +5 more
doaj   +1 more source

Herpes simplex virus interferes with amyloid precursor protein processing [PDF]

open access: yes, 2005
Background The early events underlying Alzheimer's disease (AD) remain uncertain, although environmental factors may be involved. Work in this laboratory has shown that the combination of herpes simplex virus type 1 (HSV1) in brain and carriage of the
Dobson, C.B.   +3 more
core   +4 more sources

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