Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Highest usefulness score first. Studies without a score come last.
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Although its etiology is not completely known, several factors including deficits of acetylcholine, β-amyloid deposits, τ-protein phosphorylation, oxidative stress, and neuroinflammation are considered to play significant roles in the pathophysiology of this disease.
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Alzheimer's Association Research Roundtable Fall 2015-Tau: From research to clinical development.
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Microtubule-associated protein tau becomes abnormally phosphorylated in Alzheimer's disease and other tauopathies and forms aggregates of paired helical filaments (PHF-tau).
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Transgenic Tg2576 mice overexpressing human amyloid precursor protein (hAPP) are a widely used Alzheimer's disease (AD) mouse model to evaluate treatment effects on amyloid beta (Aβ) pathology and cognition.
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Alzheimer's disease (AD) is associated with defects of synaptic connectivity.
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Microglia have been shown to contribute to the clearance of brain amyloid β peptides (Aβ), the major component of amyloid plaques, in Alzheimer's disease (AD).
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Alzheimer's disease (AD) is a biologically complex neurodegenerative dementia.
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Our data support the use of Tau aggregation inhibitors as potential drugs for the treatment of AD and other tauopathies and highlights the need for preventive treatment before onset of cognitive impairments.
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In Alzheimer's disease (AD), an extensive accumulation of extracellular amyloid plaques and intraneuronal tau tangles, along with neuronal loss, is evident in distinct brain regions.
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Further analysis of brain-derived ∼7 kDa Aβ species, the mechanism by which they assemble and the structures they form should reveal therapeutic and diagnostic opportunities.
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40/100
Mammalian cells remove misfolded proteins using various proteolytic systems, including the ubiquitin (Ub)-proteasome system (UPS), chaperone mediated autophagy (CMA) and macroautophagy.
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Alzheimer's disease (AD) is a neurodegenerative disorder characterized by loss of memory and cognitive abilities, and the appearance of amyloid plaques composed of the amyloid-β peptide (Aβ) and neurofibrillary tangles formed of tau protein.
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The ability to maintain a functional proteome, or proteostasis, declines during the ageing process.
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This biomarker discrepancy is likely due to overexpression of amyloid precursor protein in the transformed cellular models.
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40/100
The amyloid cascade hypothesis has been the prevailing hypothesis in Alzheimer's Disease research, although the final and most wanted proof i.e. fully successful anti-amyloid clinical trials in patients, is still lacking.
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Alzheimer's disease (AD) is a devastating disease characterized by synaptic and neuronal loss in the elderly.
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Proteinaceous inclusions are common hallmarks of many neurodegenerative diseases.
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Intracellular protein trafficking plays an important role in neuronal function and survival.
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We have discovered defined determinants on mis-disordered truncated tau protein which are responsible for tau oligomerisation leading to neurofibrillary degeneration.
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The severity of tau pathology in Alzheimer's disease brain correlates closely with disease progression.
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Experimental studies of Alzheimer's disease have largely depended on transgenic mice overexpressing amyloid precursor protein (APP).
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40/100
The memory-enhancing effect of IVIg reported here suggests that Aβ oligomers, effector T cells and the fractalkine pathway are potential pharmacological targets of IVIg in AD.
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Inhibitions of amyloid β (Aβ) aggregation and Aβ-haem peroxidase-like activity have received much attention because these two symptoms can be the primary targets of therapeutic strategies for Alzheimer's disease (AD).
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Current treatment options for Alzheimer's disease (AD) are limited to medications that reduce dementia symptoms.
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As the second most common age related neurodegenerative disease after Alzheimer's disease, the health, social and economic impact resulting from Parkinson's disease will continue to increase alongside the longevity of the population.
From across this topic
10 of the 1,352 studies in this topic, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Antibody-Mediated Targeting of Tau In Vivo Does Not Require Effector Function and Microglial Engagement
- Distinct neurotoxic TDP-43 fibril polymorphs are generated by heterotypic interactions with α-Synuclein
- The sleep-wake cycle regulates brain interstitial fluid tau in mice and CSF tau in humans
- Hereditary and sporadic forms of abeta-cerebrovascular amyloidosis and relevant transgenic mouse models
- The potential of microelectrode arrays and microelectronics for biomedical research and diagnostics
- TMEM55B downregulation promotes neurodegeneration in Alzheimer’s disease models
- Cellular Prion Protein Mediates the Disruption of Hippocampal Synaptic Plasticity by Soluble Tau In Vivo
- ErbB2 regulates autophagic flux to modulate the proteostasis of APP-CTFs in Alzheimer's disease
- Inhibition of mTOR by rapamycin abolishes cognitive deficits and reduces amyloid-beta levels in a mouse model of Alzheimer's disease
- Efficient in vivo delivery of antisense oligonucleotide to choroid plexus