Results 51 to 60 of about 343,599 (390)

Therapeutic Potential of Secreted Amyloid Precursor Protein APPsα

open access: yesFrontiers in Molecular Neuroscience, 2017
Cleavage of the amyloid precursor protein (APP) by α-secretase generates an extracellularly released fragment termed secreted APP-alpha (APPsα). Not only is this process of interest due to the cleavage of APP within the amyloid-beta sequence, but APPsα ...
B. Mockett   +3 more
semanticscholar   +1 more source

Neuregulin-1 Exerts Protective Effects Against Neurotoxicities Induced by C-Terminal Fragments of APP via ErbB4 Receptor

open access: yesJournal of Pharmacological Sciences, 2012
Neuregulin-1 (NRG1) plays important roles in the development and plasticity of the brain, and it is also reported to have potent neuroprotective properties.
Junghwa Ryu   +6 more
doaj   +1 more source

Proteinopathy, oxidative stress and mitochondrial dysfunction: cross talk in alzheimer’s disease and parkinson’s disease [PDF]

open access: yes, 2017
Alzheimer's disease and Parkinson's disease are two common neurodegenerative diseases of the elderly people that have devastating effects in terms of morbidity and mortality.
Chakrabarti, S.   +3 more
core   +3 more sources

Amyloid Precursor-like Protein 1 Influences Endocytosis and Proteolytic Processing of the Amyloid Precursor Protein [PDF]

open access: yesJournal of Biological Chemistry, 2006
Ectodomain shedding of the amyloid precursor protein (APP) is a key regulatory step in the generation of the Alzheimer disease amyloid beta peptide (Abeta). The molecular mechanisms underlying the control of APP shedding remain little understood but are in part dependent on the low density lipoprotein receptor-related protein (LRP), which is involved ...
Neumann, Stephanie   +6 more
openaire   +3 more sources

Amyloid precursor protein in peripheral granulocytes as a potential biomarker for Alzheimer’s disease

open access: yesBangladesh Journal of Pharmacology, 2016
The aim of this study was to assess the potential of amyloid precursor protein in peripheral granulocytes as a diagnostic biomarker for early detection of Alzheimer’s disease.
Xiaonan Wang   +4 more
doaj   +2 more sources

Cytoprotective functions of amyloid precursor protein family members in stress signaling and aging [PDF]

open access: yes, 2013
Poster presentation: Molecular Neurodegeneration: Basic biology and disease pathways Cannes, France. 10-12 September 2013. Background: The amyloid precursor protein (APP) is processed via two different metabolic pathways: the amyloidogenic and the non ...
Chang, Steffi   +4 more
core   +1 more source

Rosiglitazone ameliorates diffuse axonal injury by reducing loss of tau and up-regulating caveolin-1 expression

open access: yesNeural Regeneration Research, 2016
Rosiglitazone up-regulates caveolin-1 levels and has neuroprotective effects in both chronic and acute brain injury. Therefore, we postulated that rosiglitazone may ameliorate diffuse axonal injury via its ability to up-regulate caveolin-1, inhibit ...
Yong-lin Zhao   +5 more
doaj   +1 more source

Genetic dissection of down syndrome-associated alterations in APP/amyloid-β biology using mouse models

open access: yesScientific Reports, 2021
Individuals who have Down syndrome (caused by trisomy of chromosome 21), have a greatly elevated risk of early-onset Alzheimer’s disease, in which amyloid-β accumulates in the brain. Amyloid-β is a product of the chromosome 21 gene APP (amyloid precursor
Justin L. Tosh   +12 more
doaj   +1 more source

Traumatic Microhemorrhages Are Not Synonymous With Axonal Injury

open access: yesAnnals of Clinical and Translational Neurology, EarlyView.
ABSTRACT Diffuse axonal injury (DAI) is caused by acceleration‐deceleration forces during trauma that shear white matter tracts. Susceptibility‐weighted MRI (SWI) identifies microbleeds that are considered the radiologic hallmark of DAI and are used in clinical prognostication.
Karinn Sytsma   +9 more
wiley   +1 more source

Amyloid-β acts as a regulator of neurotransmitter release disrupting the interaction between synaptophysin and VAMP2. [PDF]

open access: yes, 2012
BACKGROUND: It is becoming increasingly evident that deficits in the cortex and hippocampus at early stages of dementia in Alzheimer's disease (AD) are associated with synaptic damage caused by oligomers of the toxic amyloid-β peptide (Aβ42).
Alifragis, P   +5 more
core   +2 more sources

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