Results 51 to 60 of about 268,148 (374)

Aβ(1-42) tetramer and octamer structures reveal edge conductivity pores as a mechanism for membrane damage

open access: yesNature Communications, 2020
Formation of amyloid-beta (Aβ) oligomer pores in the membrane of neurons has been proposed to explain neurotoxicity in Alzheimerʼs disease (AD). Here, we present the three-dimensional structure of an Aβ oligomer formed in a membrane mimicking environment,
Sonia Ciudad   +14 more
semanticscholar   +1 more source

Can insulin signaling pathways be targeted to transport Aβ out of the brain? [PDF]

open access: yesFrontiers in Aging Neuroscience, 2015
Although the causal role of Amyloid-β (Aβ) in Alzheimer's disease (AD) is unclear, it is still reasonable to expect that lowering concentrations of Aβ in the brain may decrease the risk of developing the neurocognitive symptoms of the disease. Brain capillary endothelial cells forming the blood-brain barrier (BBB) express transporters regulating the ...
Vandal, Milene   +2 more
openaire   +3 more sources

Nanomedicine Against Aβ Aggregation by β–Sheet Breaker Peptide Delivery: In Vitro Evidence

open access: yesPharmaceutics, 2019
The accumulation of amyloid β (Aβ) triggers a cascade of toxic events in Alzheimer’s disease (AD). The KLVFF peptide can interfere with Aβ aggregation. However, the peptide suffers from poor bioavailability and the inability to cross
Francesca Pederzoli   +13 more
doaj   +1 more source

Multimodal MRI-based Imputation of the Aβ+ in Early Mild Cognitive Impairment. [PDF]

open access: yes, 2014
ObjectiveTo identify brain atrophy from structural-MRI and cerebral blood flow(CBF) patterns from arterial spin labeling perfusion-MRI that are best predictors of the Aβ-burden, measured as composite 18F-AV45-PET uptake, in individuals with early mild ...
Joshi, Sarang   +3 more
core   +1 more source

Aβ degradation or cerebral perfusion? Divergent effects of multifunctional enzymes [PDF]

open access: yesFrontiers in Aging Neuroscience, 2014
There is increasing evidence that deficient clearance of β-amyloid (Aβ) contributes to its accumulation in late-onset Alzheimer disease (AD). Several Aβ-degrading enzymes, including neprilysin (NEP), endothelin-converting enzyme (ECE), and angiotensin-converting enzyme (ACE) reduce Aβ levels and protect against cognitive impairment in mouse models of ...
Miners, J. Scott   +6 more
openaire   +3 more sources

The role and therapeutic targeting of α-, β- and γ-secretase in Alzheimer's disease [PDF]

open access: yes, 2015
Alzheimer's disease (AD) is the most common form of dementia in the elderly and its prevalence is set to increase rapidly in coming decades. However, there are as yet no available drugs that can halt or even stabilize disease progression. One of the main
Baillie, George S.   +3 more
core   +1 more source

A mechanistic hypothesis for the impairment of synaptic plasticity by soluble Aβ oligomers from Alzheimer’s brain

open access: yesJournal of Neurochemistry, 2020
It is increasingly accepted that early cognitive impairment in Alzheimer's disease results in considerable part from synaptic dysfunction caused by the accumulation of a range of oligomeric assemblies of amyloid β‐protein (Aβ).
Shaomin Li, D. Selkoe
semanticscholar   +1 more source

Alzheimer's Aβ fused to green fluorescent protein induces growth stress and a heat shock response [PDF]

open access: yesFEMS Yeast Research, 2007
The 42 amino acid Alzheimer's Abeta peptide is involved in the progression of Alzheimer's disease. Here we describe the effects of intracellular Abeta, produced through its attachment to either end of a green fluorescent protein, in yeast. Cells producing Abeta exhibited a lower growth yield and a heat shock response, showing that Abeta fusions promote
Caine, Jo   +6 more
openaire   +3 more sources

Coffee and Caffeine Potentiate the Antiamyloidogenic Activity of Melatonin via Inhibition of Aβ Oligomerization and Modulation of theTau-Mediated Pathway in N2a/APP Cells [Retraction]

open access: yesDrug Design, Development and Therapy, 2022
Zhang LF, Zhou ZW, Wang ZH, et al. Drug Des Devel Ther. 2014;9:241–272. The Editor and Publisher of Drug Design, Development and Therapy wish to retract the published article.
Zhang L   +6 more
doaj  

Controlled cortical impact traumatic brain injury in 3xTg-AD mice causes acute intra-axonal amyloid-β accumulation and independently accelerates the development of tau abnormalities [PDF]

open access: yes, 2011
Alzheimer\u27s disease (AD) is a neurodegenerative disorder characterized pathologically by progressive neuronal loss, extracellular plaques containing the amyloid-β (Aβ) peptides, and neurofibrillary tangles composed of hyperphosphorylated tau proteins.
Brody, David L   +3 more
core   +2 more sources

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