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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Tauopathies are clinicopathological entities with increased and pathological deposition in glia and/or neurons of hyperphosphorylated aggregates of the microtubule-binding protein tau.
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Alzheimer's disease (AD), the leading cause of dementia, is a growing health issue with very limited treatment options.
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41/100
Positron emission tomography (PET) imaging allows monitoring the progression of amyloid aggregation in the living brain. [18F]-Flortaucipir is the only approved PET tracer compound for the visualisation of tau aggregation.
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Mutations in a microglia-associated gene TREM2 increase the risk of Alzheimer's disease.
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During Alzheimer's (AD), tau protein suffers from abnormal post-translational modifications, including cleaving by caspase-3.
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Presenilin 1 (PSEN1) is a part of the gamma secretase complex with several interacting substrates, including amyloid precursor protein (APP), Notch, adhesion proteins and beta catenin.
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A mouse model of tauopathy and human myocardial and brain tissue from patients with HF, AD, and controls was employed in this study.
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The global north is facing an unprecedented rise in the prevalence of neurodegenerative diseases.
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Pathogenic α-synuclein and tau are critical drivers of neurodegeneration, and their mutations cause neuronal loss in patients.
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The disturbance in mitochondrial functions and homeostasis are the major features of neuron degenerative conditions, like Parkinson's disease, Amyotrophic Lateral Sclerosis, and Alzheimer's disease, along with protein misfolding.
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Cellular deposition of protein aggregates, one of the hallmarks of neurodegeneration, disrupts cellular functions and leads to neuronal death.
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Mutations in the Presenilin genes (PSEN1 and PSEN2) are the major cause of familial Alzheimer's disease (AD), highlighting the importance of Presenilin (PS) in AD pathogenesis.
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Tau pathology is essential in the pathogenesis of Alzheimer's disease (AD) and related tauopathies.
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The homeostasis of cellular proteins, or proteostasis, is critical for neuronal function and for brain processes, including learning and memory.
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41/100
TTR (transthyretin) strikes a neuroprotective function in the prevention of amyloid-β (Aβ) deposition in Alzheimer disease (AD).
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Alzheimer's disease (AD) is an age-related neurodegenerative disease characterized by tau aggregating into neurofibrillary tangles.
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Synaptic dysfunction caused by soluble β-amyloid peptide (Aβ) is a hallmark of early-stage Alzheimer's disease (AD), and is tightly linked to cognitive decline.
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Probabilistic and parsimony-based arguments regarding available genetics data are used to propose that Hardy and Higgin's amyloid cascade hypothesis is valid but is commonly interpreted too narrowly to support, incorrectly, the primacy of the amyloid-β peptide (Aβ) in driving Alzheimer's disease pathogenesis.
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Tauopathies are heterogeneous clinicopathological entities characterized by abnormal neuronal and/or glial inclusions of the microtubule-binding protein tau.
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With the growth of the aging population, more age-related diseases endanger the health of the elderly, and therefore more research attention has been put on Alzheimer's disease and dementia.
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We found several deregulated biological processes linked to the synapse. miR-101a-3p was validated as a synaptic miRNA upregulated in aSyn Tg mice and in the cortex of dementia with Lewy bodies patients.
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Alzheimer's disease (AD) is a multivariate and diversified disease and affects the most sensitive areas of the brain, the cerebral cortex, and the hippocampus.
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41/100
Antisense oligonucleotide (ASO) therapy for neurological disease has been successful in clinical settings and its potential has generated hope for Alzheimer's disease (AD).
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Alzheimer's disease (AD) is characterised by the presence of extracellular amyloid plaques in the brain.
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Accumulation of neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau is a histopathological hallmark of Alzheimer's disease (AD) and related tauopathies.
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.
- Complete protein characterization using top-down mass spectrometry and ultraviolet photodissociation
- Alpha‐synuclein p.H50Q, a novel pathogenic mutation for Parkinson's disease
- Precortical Phase of Alzheimer's Disease (AD)-Related Tau Cytoskeletal Pathology
- Molecular mechanisms of neurodegeneration in Alzheimer's disease
- Apolipoprotein E isoform does not influence trans-synaptic spread of tau pathology in a mouse model
- Secretion of beta-amyloid precursor protein cleaved at the amino terminus of the beta-amyloid peptide
- Loss-of-function mutations in the ATP13A2/PARK9 gene cause complicated hereditary spastic paraplegia (SPG78)
- Structural Insights and Biological Effects of Glycogen Synthase Kinase 3-specific Inhibitor AR-A014418
- Structural and kinetic basis for the selectivity of aducanumab for aggregated forms of amyloid-β
- Axonal mitochondrial transport and potential are correlated