Results 131 to 140 of about 94,035 (378)

Golgi Fragmentation in Alzheimer’s Disease

open access: yesFrontiers in Neuroscience, 2015
The Golgi apparatus is an essential cellular organelle for post-translational modifications, sorting, and trafficking of membrane and secretory proteins. Proper functionality of the Golgi requires the formation of its unique cisternal-stacking morphology.
Gunjan eJoshi   +3 more
doaj   +1 more source

Correlating familial Alzheimer’s disease gene mutations with clinical phenotype [PDF]

open access: yes, 2010
Alzheimer’s disease (AD) causes devastating cognitive impairment and an intense research effort is currently devoted to developing improved treatments for it.
Rossor, M.N., Ryan, N.S.
core   +1 more source

Fe65 Is Phosphorylated on Ser289 after UV-Induced DNA Damage [PDF]

open access: yes, 2016
Fe65 undergoes a phosphatase-sensitive gel mobility shift after DNA damage, consistent with protein phosphorylation. A recent study identified Ser228 as a specific site of phosphorylation, targeted by the ATM and ATR protein kinases, with phosphorylation
Blain, Peter G.   +3 more
core   +2 more sources

Wading pools and fading memories – place navigation in transgenic mouse models of Alzheimer’s disease

open access: yesFrontiers in Aging Neuroscience, 2012
The Morris swim navigation task (‘water maze’) has been a primary research tools to assess hippocampal delpendent spatial learning and memory is rodents for three decades. Originally developed for rats, its application to mouse studies has been a tedious
Heikki eTanila
doaj   +1 more source

New Insights in the Amyloid-Beta Interaction with Mitochondria

open access: yesJournal of Aging Research, 2012
Biochemical and morphological alterations of mitochondria may play an important role in the pathogenesis of Alzheimer’s disease (AD). Particularly, mitochondrial dysfunction is a hallmark of amyloid-beta-induced neuronal toxicity in Alzheimer’s disease ...
Carlos Spuch   +2 more
doaj   +1 more source

Framework for assessing the risk to a field from fraudulent researchers: A case study of Alzheimer's disease

open access: yesJournal of the Association for Information Science and Technology, EarlyView.
Abstract Concerns over research integrity are rising, with increasing attention to potential threats from untrustworthy authors. We established a framework to gauge the potential negative influence of researchers potentially engaged in misconduct. The field of Alzheimer's disease (AD) research has been a focal point of these worries. This study aims to
Chaoqun Ni, B. Ian Hutchins
wiley   +1 more source

Potential contribution of exosomes to the prion-like propagation of lesions in Alzheimer’s disease

open access: yesFrontiers in Physiology, 2012
Since the discovery of prion diseases, the concept that a transmissible pathogen could be a protein has emerged. As such, this transmissible protein agent can transfer its pathological mis-folded shape to the same but normally folded protein thus leading
Valerie eVingtdeux   +2 more
doaj   +1 more source

Mechanical Characterization of Amyloid Fibrils Using Coarse-Grained Normal Mode Analysis [PDF]

open access: yesAdvanced Functional Materials 2011, 2011
Recent experimental studies have shown that amyloid fibril formed by aggregation of {\beta} peptide exhibits excellent mechanical properties comparable to other protein materials such as actin filaments and microtubules. These excellent mechanical properties of amyloid fibrils are related to their functional role in disease expression.
arxiv  

Mitochondria and Endoplasmic Reticulum Contact Site as a Regulator of Proteostatic Stress Responses in Neurodegenerative Diseases

open access: yesBioEssays, EarlyView.
Recent findings indicate that mitochondria‐associated membranes (MAMs), where the endoplasmic reticulum directly contacts the mitochondria, are a novel microdomain essential for cellular homeostasis, including proteostasis. We summarize the disruption of protein homeostasis and MAM alteration in neurodegenerative diseases, then discuss challenges and ...
Seiji Watanabe, Koji Yamanaka
wiley   +1 more source

APP Causes Hyperexcitability in Fragile X Mice

open access: yesFrontiers in Molecular Neuroscience, 2016
Amyloid-beta protein precursor (APP) and metabolite levels are altered in fragile X syndrome (FXS) patients and in the mouse model of the disorder, Fmr1KO mice.
Cara Jean Westmark   +8 more
doaj   +1 more source

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