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, a group of neurodegenerative disorders, are characterized by disrupted homeostasis of the microtubule binding protein tau.
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Cognitive dysfunction and dementia are critical symptoms of Lewy Body dementias (LBD).
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Neurodegenerative disorders are devastating disorders characterized by gradual loss of neurons and cognition or mobility impairment.
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Neuronal loss is the central issue in Alzheimer's disease (AD), yet no treatment developed so far can halt AD-associated neurodegeneration.
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Sleep apnea is regarded as an important risk factor in the pathogenesis of Alzheimer disease (AD).
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by memory impairment, a loss of cholinergic neurons, and cognitive decline that insidiously progresses to dementia.
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The hypothesis that neurodegenerative diseases are proteinopathies due to toxic effect of different underlying proteins, such as amyloid-beta and 3+4R-tau in Alzheimer's disease (AD) and alpha-synuclein in Parkinson's disease (PD), while still controversial is supported by several studies in the literature.
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Cortical synaptic loss has emerged as an early abnormality in Alzheimer's disease (AD) with a strong relationship to cognitive performance.
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Spinocerebellar ataxia type 3 (SCA3) is the most common dominantly inherited ataxia.
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Intersectin (ITSN) is a multi-domain scaffold protein with a diverse array of functions including regulation of endocytosis, vesicle transport, and activation of various signal transduction pathways.
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Alzheimer's disease (AD) and non-AD tauopathies such as chronic traumatic encephalopathy (CTE), progressive supranuclear palsy (PSP), and corticobasal degeneration (CBD) are characterized by the abnormal aggregation of three-repeat (3R) and/or four-repeat (4R) tau isoforms.
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Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are devastating neurodegenerative diseases with no effective cure.
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Tau is a microtubule-associated protein essential for microtubule assembly and stability in neurons.
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Alzheimer's disease (AD) is a significant 21st-century public health challenge.
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Amyloid-β (Aβ) plaques and neurofibrillary tangles containing phosphorylated tau protein are major hallmarks of Alzheimer's disease (AD).
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Aggregation of tau protein is a pathological hallmark of Alzheimer's disease and other neurodegenerative tauopathies.
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Our understanding of stress granule (SG) biology has deepened considerably in recent years, and with this, increased understanding of links has been made between SGs and numerous neurodegenerative diseases.
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Apolipoprotein E (APOE) is a strong genetic risk factor for late-onset Alzheimer's disease (LOAD).
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Intraneuronal dysproteostasis and extraneuronal microenvironmental abnormalities in Alzheimer's disease (AD) collectively culminate in neuronal deterioration.
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Alzheimer's disease (AD) is classically characterized by senile plaques and neurofibrillary tangles (NFTs).
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However, while Aβ may contribute to disease, genetic, clinical, imaging and biochemical data suggest a more complex aetiology.
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We have recently shown that multiple tRNA synthetase inhibitors can greatly increase lifespan in multiple models by acting through the conserved transcription factor ATF4.
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Alzheimer's disease (AD) is the most common chronic neurodegenerative disease worldwide.
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The deposition of highly phosphorylated and aggregated tau is a characteristic of tauopathies, including Alzheimer's disease.
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Extensive studies indicate that β-amyloid (Aβ) aggregation is pivotal for Alzheimer's disease (AD) progression; however, cumulative evidence suggests that Aβ itself is not sufficient to trigger AD-associated degeneration, and whether other additional pathological factors drive AD pathogenesis remains unclear.
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.
- Curcumin loaded-PLGA nanoparticles conjugated with Tet-1 peptide for potential use in Alzheimer's disease
- Prolonged Drug-Releasing Fibers Attenuate Alzheimer's Disease-like Pathogenesis
- Semaglutide-mediated protection against Aβ correlated with enhancement of autophagy and inhibition of apotosis
- Early astrocytic atrophy in the entorhinal cortex of a triple transgenic animal model of Alzheimer's disease
- LATS2 modulates synaptic organization and function by regulating actin dynamics
- Mutant-Huntingtin Molecular Pathways Elucidate New Targets for Drug Repurposing
- Impairing the mitochondrial fission and fusion balance: a new mechanism of neurodegeneration
- Riluzole reduces amyloid beta pathology, improves memory, and restores gene expression changes in a transgenic mouse model of early-onset Alzheimer's disease
- Dimerization of the transmembrane domain of amyloid precursor proteins and familial Alzheimer's disease mutants
- Dementia with Lewy bodies: emerging drug targets and therapeutics