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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Alpha-synuclein (αS) is the major constituent of Lewy bodies and a pathogenic hallmark of all synucleinopathathies, including Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA).
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[ 18 F]PI-2620 was selected for clinical validation.
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The microtubule-associated protein tau is an attractive therapeutic target for the treatment of Alzheimer's disease and related tauopathies as its aggregation strongly correlates with disease progression and is considered a key mediator of neuronal toxicity.
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The amyloid-β (Aβ) peptide and tau protein are thought to play key neuropathogenic roles in Alzheimer's disease (AD).
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41/100
Parkinson's disease (PD) is the second most common degenerative disorder.
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There are few disease-modifying therapeutics for neurodegenerative diseases, but successes on the development of antisense oligonucleotide (ASO) therapeutics for spinal muscular atrophy and Duchenne muscular dystrophy predict a robust future for ASOs in medicine.
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Alzheimer's disease (AD) is a growing global health concern with a massive impact on affected individuals and society.
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41/100
Hundreds of proteins are known to be citrullinated and hypercitrullination is associated with autoimmune diseases including rheumatoid arthritis (RA), lupus, ulcerative colitis (UC), Alzheimer's disease, multiple sclerosis (MS), and certain cancers.
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Accumulation of damaged mitochondria is a hallmark of aging and age-related neurodegeneration, including Alzheimer's disease (AD).
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In Alzheimer's disease (AD), early synaptic dysfunction is associated with the increased oligomeric amyloid-beta peptide, which causes NMDAR-dependent synaptic depression and spine elimination.
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Porphyromonas gingivalis , the keystone pathogen in chronic periodontitis, was identified in the brain of Alzheimer's disease patients.
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41/100
Intramembrane proteolysis of transmembrane substrates by the presenilin-γ-secretase complex is preceded and regulated by shedding of the substrate's ectodomain by α- or β-secretase.
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In BriefIn the search for biomarkers of synapse loss associated with Alzheimer's disease (AD), we used shotgun proteomics to identify a panel of 9 synaptic proteins detectable in human cerebrospinal fluid (CSF).Expression at the human synapse was verified using super resolution microscopy.
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Human mini-brains (MB) are cerebral organoids that recapitulate in part the complexity of the human brain in a unique three-dimensional in vitro model, yielding discrete brain regions reminiscent of the cerebral cortex.
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Based on the improved efficacy/safety profile in non-clinical models of SAR228810, a first-in-man single and multiple dose administration clinical study has been initiated in AD patients.
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Alzheimer's disease is a neurodegenerative disorder mainly characterized by β-amyloid deposit and tau hyperphosphorylation with no curative treatments.
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Tau protein accumulation is the most common pathology among degenerative brain diseases, including Alzheimer's disease (AD), progressive supranuclear palsy (PSP), traumatic brain injury (TBI), and over twenty others.
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The typical abnormalities observed in the brain of Alzheimer's disease (AD) patients include synaptic alterations, neuronal death, brain inflammation, and the accumulation of protein aggregates in the form of amyloid plaques and neurofibrillary tangles.
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Alzheimer's disease (AD) represents a major healthcare burden with no effective treatment.
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App NL/NL and App NL-G-F/NL-G-F mice exhibit behavioral changes associated with non-cognitive, emotional domains before the onset of definitive cognitive deficits.
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The incidences of presbycusis and dementia are high among geriatric diseases.
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Progressive accumulation of misfolded amyloid proteins in intracellular and extracellular spaces is one of the principal reasons for synaptic damage and impairment of neuronal communication in several neurodegenerative diseases.
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Misfolded and hyperphosphorylated tau accumulates in several neurodegenerative disorders including Alzheimer's disease, frontotemporal dementia with Parkinsonism, corticobasal degeneration, progressive supranuclear palsy, Down syndrome, and Pick's disease.
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41/100
Aducanumab, a human-derived antibody targeting amyloid-β (Aβ), is in Phase 3 clinical trials for the treatment of Alzheimer's disease.
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Amyloid pathology occurs early in Alzheimer's disease (AD), and has therefore been the focus of numerous studies.
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.
- Mechanisms of neurodegeneration - Insights from familial Alzheimer's disease
- Protein degradation-associated mechanisms that are affected in Alzheimer´s disease
- Immunochemical and biochemical characterization of tau proteins in normal and Alzheimer's disease brains with Alz 50 and Tau-1
- Peptide-Based Molecular Strategies To Interfere with Protein Misfolding, Aggregation, and Cell Degeneration
- miR-101a-3p Impairs Synaptic Plasticity and Contributes to Synucleinopathy
- Anti-alpha synuclein and anti-tau immunotherapies: Can a cocktail approach work?
- Highly specific and selective anti-pS396-tau antibody C10.2 targets seeding-competent tau
- Pathogenic PS1 phosphorylation at Ser367
- The amyloid cascade hypothesis for Alzheimer's disease: an appraisal for the development of therapeutics
- Current and future therapeutic strategies for Alzheimer's disease: an overview of drug development bottlenecks