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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Alzheimer's disease (AD) is a progressive neurodegenerative condition characterized by tau pathology and accumulations of neurofibrillary tangles (NFTs) along with amyloid-beta (Aβ).
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There are few treatments that slow neurodegeneration in Alzheimer's disease (AD), and while therapeutic antibodies are being investigated in clinical trials for AD treatment, their access to the central nervous system is restricted by the blood-brain barrier.
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Immunotherapy against amyloid-beta (Aβ) is a promising option for the treatment of Alzheimer's disease (AD).
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Presenilin-1 (PSEN1) has been verified as an important causative factor for early onset Alzheimer's disease (EOAD).
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These results suggest that the targeted methylation of APP via dCas9-Dnmt3a treatment can be a potential therapeutic strategy for AD.
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Alzheimer's disease is a neurodegenerative disease that accounts for most of the 50-million dementia cases worldwide in 2018.
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Amyloid plaques contain many proteins in addition to beta amyloid (Aβ).
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Alzheimer's disease (AD) is the most common neurodegenerative disease in the elderly worldwide.
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Neurodegenerative disorders are primarily characterized by neuron loss.
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Synaptic abnormalities are a cardinal feature of Alzheimer's disease (AD) that are known to arise as the disease progresses.
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A reduced removal of dysfunctional mitochondria is common to aging and age-related neurodegenerative pathologies such as Alzheimer's disease (AD).
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43/100
RNA therapeutics comprise a diverse group of oligonucleotide-based drugs such as antisense oligonucleotides (ASOs), small interfering RNAs (siRNAs), and short hairpin RNAs (shRNAs) that can be designed to selectively interact with drug targets currently undruggable with small molecule-based drugs or monoclonal antibodies.
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Both the replication of protein aggregates and their spreading throughout the brain are implicated in the progression of Alzheimer’s disease (AD).
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Microtubule-associated protein tau is abnormally aggregated in neuronal and glial cells in a range of neurodegenerative diseases that are collectively referred to as tauopathies.
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Alzheimer's disease (AD) is a progressive neurodegenerative disease with no cure.
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The ability to investigate therapeutic interventions in animal models of neurodegenerative diseases depends on extensive characterization of the model(s) being used.
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Chaperone-mediated autophagy (CMA) is a lysosome-dependent selective degradation pathway implicated in the pathogenesis of cancer and neurodegenerative diseases.
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A large body of clinical and nonclinical evidence supports the role of neurotoxic soluble beta amyloid (amyloid, Aβ) oligomers as upstream pathogenic drivers of Alzheimer's disease (AD).
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Phosphorylation is one of the most prevalent post-translational modifications found in aggregated tau isolated from Alzheimer's disease (AD) patient brains.
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Dysfunction of the endolysosomal-autophagy network is emerging as an important pathogenic process in Alzheimer's disease.
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Precursor messenger RNA (pre-mRNA) splicing is a fundamental step in eukaryotic gene expression that systematically removes non-coding regions (introns) and ligates coding regions (exons) into a continuous message (mature mRNA).
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Increasing life expectancy has led to an aging population, which has consequently increased the prevalence of dementia.
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43/100
Tau is a microtubule associated protein in the brain that aggregates in Alzheimer's disease to form pathological tangles and neurites.
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Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are two clinically distinct classes of neurodegenerative disorders.
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Mitochondrial dysfunction is an established hallmark of aging and neurodegenerative disorders such as Down syndrome (DS) and Alzheimer's disease (AD).
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.
- Amyloid precursor protein processing and Alzheimer's disease
- Control of mitochondrial biogenesis and function by the ubiquitin-proteasome system
- Mapping post-translational modifications across amyloid-β deposits in Alzheimer’s disease: A neuropathologic survey with in vitro functional analysis of nitration
- Role of genes linked to sporadic Alzheimer's disease risk in the production of β-amyloid peptides
- Multimerization of TREM2 is impaired by Alzheimer's disease-associated variants
- (-)-epigallocatechin-3-gallate (EGCG) maintains kappa-casein in its pre-fibrillar state without redirecting its aggregation pathway
- Neurodegeneration and the ordered assembly of α-synuclein
- Statins reduce neuronal alpha-synuclein aggregation in in vitro models of Parkinson's disease
- Isoform-specific binding of apolipoprotein E to beta-amyloid
- Amyloid tracers binding sites in autosomal dominant and sporadic Alzheimer's disease