When, where and how? Focus on neuronal calcium dysfunctions in Alzheimer's Disease. [PDF]
, 2016 Alzheimer\u2019s disease (AD), since its characterization as a precise form of dementia with its own pathological hallmarks, has captured scientists\u2019 attention because of its complexity.
AGOSTINI, MARIO, FASOLATO, CRISTINA
core +1 more source
QBP1 Peptide as a Potential Anti‐Amyloidogenic Therapy for Type 2 Diabetes: An In Vitro Study
Advanced Science, EarlyView.The anti‐amyloidogenic peptide QBP1 effectively halts human islet amyloid polypeptide (hIAPP) aggregation, preventing the formation of toxic β‐structured intermediates. Through a combination of biophysical assays, molecular dynamics, and cell‐based studies, QBP1 is shown to preserve β‐cell viability and metabolic homeostasis, positioning it as a ...
María M. Tejero‐Ojeda +8 more
wiley +1 more source
A Physiological Role for Amyloid Beta Protein: Enhancement of Learning and Memory [PDF]
, 2008 Amyloid beta protein (A[beta]) is well recognized as having a significant role in the pathogenesis of Alzheimer's disease (AD). The reason for the presence of A[beta] and its physiological role in non-disease states is not clear.
John Morley +5 more
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Stabilizing the Retromer Complex in a Human Stem Cell Model of Alzheimer's Disease Reduces TAU Phosphorylation Independently of Amyloid Precursor Protein. [PDF]
, 2018 Developing effective therapeutics for complex diseases such as late-onset, sporadic Alzheimer's disease (SAD) is difficult due to genetic and environmental heterogeneity in the human population and the limitations of existing animal models. Here, we used
Fong, Lauren K +5 more
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Amyloid Beta Peptide Slows Down Sensory-Induced Hippocampal Oscillations [PDF]
International Journal of Peptides, 2012 Alzheimer’s disease (AD) progresses with a deterioration of hippocampal function that is likely induced by amyloid beta (Aβ) oligomers. Hippocampal function is strongly dependent on theta rhythm, and disruptions in this rhythm have been related to the reduction of cognitive performance in AD. Accordingly, both AD patients and AD-transgenic mice show an
Peña-Ortega, Fernando +1 more
openaire +2 more sources
The Uppsala APP Mutation Promotes Wild‐Type Amyloid‐β Aggregation and Deposition In Vivo
Advanced Science, EarlyView.We investigated in vivo cross‐seeding of amyloid‐β (Aβ) isoforms in transgenic mice co‐expressing wild‐typeAβ and the Uppsala‐mutant Aβ variant (AβUpp), lacking six central residues. Weleveraged MALDI‐MS imaging and hyperspectral microscopy to follow spatio‐temporalAβ deposition.
Junyue Ge +14 more
wiley +1 more source
The Beta Amyloid Dysfunction (BAD) Hypothesis for Alzheimer’s Disease
Frontiers in Neuroscience, 2019 Beta amyloid, Aβ 1–42, originally named as Amyloid A4 protein, is one of the most investigated peptides in neuroscience and has attracted substantial interest since its discovery as the main insoluble fibril-type protein in cerebrovascular amyloid ...
Heinz Hillen
doaj +1 more source
cAMP-Inhibits Cytoplasmic Phospholipase A(2) and Protects Neurons against Amyloid-beta-Induced Synapse Damage [PDF]
, 2015 A key event in Alzheimer’s disease (AD) is the production of amyloid-β (Aβ) peptides and the loss of synapses. In cultured neurons Aβ triggered synapse damage as measured by the loss of synaptic proteins. α-synuclein (αSN), aggregates of which accumulate
Bate, C, Williams, A
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Accumulation of Innate Amyloid Beta Peptide in Glioblastoma Tumors [PDF]
International Journal of Molecular Sciences, 2019 Immunostaining with specific antibodies has shown that innate amyloid beta (Aβ) is accumulated naturally in glioma tumors and nearby blood vessels in a mouse model of glioma. In immunofluorescence images, Aβ peptide coincides with glioma cells, and enzyme-linked immunosorbent assay (ELISA) have shown that Aβ peptide is enriched in the membrane protein ...
Lilia Y. Kucheryavykh +5 more
openaire +2 more sources
Neuid: A Novel Neuron‐Enriched LncRNA that Connects Epigenetic Gene Silencing to Alzheimer's Disease
Advanced Science, EarlyView.ABSTRACT The increasing evidence that non‐coding RNAs can become deregulated during pathogenesis is dramatically expanding the space for drug discovery beyond the protein‐coding genome. Long noncoding RNAs (lncRNAs) are emerging as key regulators of cellular function, yet most remain uncharacterized.
Ranjit Pradhan +17 more
wiley +1 more source