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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Animal models aim to replicate the symptoms, the lesions or the cause(s) of Alzheimer disease.
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43/100
The A disintergin and metalloprotease (ADAM) superfamilies play important roles in angiogenesis, development, and tumorigenesis.
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In an effort to examine changes that precede synapse loss, we have measured amyloid-beta and a series of damage markers in the synaptic compartment of Alzheimer's disease (AD) cases.
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43/100
Filamentous tau inclusions in neurons and glia are neuropathological hallmarks of sporadic and familial tauopathies.
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Mutations in the human tau gene cause frontotemporal dementia and Parkinsonism associated with chromosome 17 (FTDP-17).
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We quantified the amount of amyloid beta-peptide (Abeta) immunoreactivity as well as amyloid deposits in a large cohort of transgenic mice overexpressing the V717F human amyloid precursor protein (APP(V717F+/-) TG mice) with no, one, or two mouse apolipoprotein E (Apoe) alleles at various ages.
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43/100
The proteins investigated in this study are present in the human retina.
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Activity of the free radical scavenging enzyme, superoxide dismutase (SOD-1), was determined in fibroblast cell lines derived from familial Alzheimer's patients, trisomy 21 patients and normal controls.
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The accumulation of hyperphosphorylated tau protein aggregates is a key pathogenic event in Alzheimer's disease (AD) and induces mitochondrial dysfunction and reactive oxygen species overproduction.
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Neurodegenerative disorders, such as Alzheimer's disease (AD) or Huntington's disease (HD), are linked to protein aggregate neurotoxicity.
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The spectrum of neurodegenerative diseases known today is quite extensive.
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Over the last decade, there has been a growing interest in intrabodies and their therapeutic potential.
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41/100
Alzheimer's disease (AD) represents the most frequent type of dementia worldwide, and aging is the most important risk factor for the sporadic form of the pathology.
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To simply and rapidly detect the highly phosphorylated tau protein at threonine 217 (p-tau217) as a precautionary measure against Alzheimer's disease and distinguish it from other neurodegenerative diseases, a novel immunosensor was prepared using luminol as the electrochemiluminescent (ECL) sensing probe reinforced by Au-Cu nanoparticles (Au-Cu NPs).
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Triggering receptor expressed on myeloid cells 2 (TREM2), a pattern recognition receptor abundantly expressed on microglia, has been identified as one of the risk factors for Alzheimer's disease (AD).
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Alzheimer's disease (AD) is characterized by the accumulation of misfolded amyloid-beta and tau proteins.
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Tauopathies are a group of neurodegenerative disorders characterized by the aggregation of the microtubule-associated protein tau.
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Autosomal dominant Alzheimer's disease (ADAD) is a rare early-onset form of Alzheimer's disease, caused by dominant mutations in one of three genes: presenilin 1, presenilin 2, and amyloid β precursor protein (APP).
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Neurodegenerative diseases (NDDs) like Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS) are defined by a myriad of complex aetiologies.
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Recent Aβ-immunotherapy trials have yielded the first clear evidence that removing aggregated Aβ from the brains of symptomatic patients can slow the progression of Alzheimer's disease.
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Increasing evidence implicates decreased energy metabolism and mitochondrial dysfunctions among the earliest pathogenic events of Alzheimer's disease (AD).
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A new class of compounds inhibiting de-O-glycosylation of proteins has been identified.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by the accumulation of Aβ plaques and neurofibrillary tangles, resulting in synaptic loss and neurodegeneration.
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41/100
A key hallmark of Alzheimer's disease (AD) is the accumulation of hyperphosphorylated tau in neurofibrillary tangles.
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SRC homology 3 (SH3) domains are fundamental modules that enable the assembly of protein complexes through physical interactions with a pool of proline-rich/noncanonical motifs from partner proteins.
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-PEG nanoparticles conjugated with B6 peptide for potential use in Alzheimer's disease
- The Alzheimer's A beta -peptide is deposited at sites of complement activation in pathologic deposits associated with aging and age-related macular degeneration
- Metabotropic glutamate receptor 5 is a coreceptor for Alzheimer aβ oligomer bound to cellular prion protein
- Microglial internalization and degradation of pathological tau is enhanced by an anti-tau monoclonal antibody
- GSK-3alpha regulates production of Alzheimer's disease amyloid-beta peptides
- Apolipoprotein E Interferes with IAPP Aggregation and Protects Pericytes from IAPP-Induced Toxicity
- A Chaperome Subnetwork Safeguards Proteostasis in Aging and Neurodegenerative Disease
- APP mouse models for Alzheimer's disease preclinical studies
- Tau fibrils evade autophagy by excessive p62 coating and TAX1BP1 exclusion
- Molecular structure of amyloid fibrils: insights from solid-state NMR