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 neurodegenerative disorder accompanied by severe progressive memory and cognitive impairment.
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Cell adhesion molecules (CAMs) have a pivotal role in building and maintaining synaptic structures during brain development participating in axonal elongation and pathfinding, glial guidance of neuronal migration, as well as myelination.
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Multiple cellular changes have been identified as being involved in Alzheimer's disease (AD) pathogenesis, including mitochondrial damage, synaptic loss, amyloid beta (Aβ) production and/or accumulation, inflammatory responses, and phosphorylated tau formation and/or accumulation.
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39/100
Synaptic dysfunction has been recognized as an early feature occurring at the onset of Alzheimer's disease (AD).
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Age-related cataracts are frequently associated with degenerative changes in the ocular lens including the aggregation of proteins - mainly crystallins, but also other proteins including amyloids (Aβ) leading to the hypothesis that cataracts could be used as "biomarkers" for Alzheimer disease.
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To elucidate the role of Tau isoforms and post-translational modification (PTM) stoichiometry in Alzheimer's disease (AD), we generated a high-resolution quantitative proteomics map of 95 PTMs on multiple isoforms of Tau isolated from postmortem human tissue from 49 AD and 42 control subjects.
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Our results provide a clue for the hypothesis that autophagy enhancement and apoptosis inhibition may be involved in the effect of semaglutide to protect against Aβ 25-35 .
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The amyloid cascade hypothesis, according to which the self-assembly of amyloid-β peptide (Aβ) is a causative process in Alzheimer's disease, has driven many therapeutic efforts for the past 20 years.
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Alzheimer's disease is one of the most common causes of dementia.
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The global epidemic of Alzheimer disease (AD) is worsening, and no approved treatment can revert or arrest progression of this disease.
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Familial Alzheimer's disease (fAD) results from mutations in the amyloid precursor protein (APP) and presenilin (PSEN1 and PSEN2) genes.
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Complement pathway overactivation can lead to neuronal damage in various neurological diseases.
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Antisense oligonucleotides represent a novel therapeutic platform for the discovery of medicines that have the potential to treat most neurodegenerative diseases.
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Ageing is a major risk factor for the development of many diseases, prominently including neurodegenerative disorders such as Alzheimer disease and Parkinson disease.
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Direct measurements of lysosomal pH uncovered a significant elevation (0.6 units) as a basis for slowed LC3 turnover and the inactivation of cathepsin D and other lysosomal hydrolases known to be unstable or less active when lysosomal pH is persistently elevated.
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Alzheimer's disease (AD) has been a global concern for years due to its severe implications that affects the quality of life of the patients.
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The aggregation of proteins into amyloid fibrils and their deposition into plaques and intracellular inclusions is the hallmark of amyloid disease.
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Synapse loss and Tau pathology are hallmarks of Alzheimer's disease (AD) and other tauopathies, but how Tau pathology causes synapse loss is unclear.
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Intracellular neurofibrillary tangles (NFTs) composed of tau protein are a neuropathological hallmark of several neurodegenerative diseases, the most common of which is Alzheimer's disease (AD).
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The dosage of the serine threonine kinase DYRK1A is critical in the central nervous system (CNS) during development and aging.
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Neurodegenerative diseases pose a substantial socioeconomic burden on society.
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A major feature of Alzheimer's disease (AD) pathology is the plaque composed of aggregated amyloid-β (Aβ) peptide.
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Proteolytic removal of membrane protein ectodomains (ectodomain shedding) is a post-translational modification that controls levels and function of hundreds of membrane proteins.
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Alzheimer disease (AD) is the most common form of dementia.
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Adipose-derived stem cells (ADSC) have a therapeutic potential for the treatment of neurodegenerative disorders such as Alzheimer's disease (AD).
From across this topic
9 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 9. The same 9 appear here every time.
- Magnetic Resonance Imaging in Tauopathy Animal Models
- Monoclonal antibody AT8 recognises tau protein phosphorylated at both serine 202 and threonine 205
- Apolipoprotein E4: a causative factor and therapeutic target in neuropathology, including Alzheimer's disease
- Control of peripheral nerve myelination by the beta-secretase BACE1
- ABC Transporter C1 Prevents Dimethyl Fumarate from Targeting Alzheimer's Disease
- Emerging amyloid and tau targeting treatments for Alzheimer's disease
- Brain region- and solubility-dependent proteomic signatures of neurofibrillary tangle pathology in Alzheimer’s disease
- A fluid biomarker reveals loss of TDP-43 splicing repression in presymptomatic ALS-FTD
- Presenilins regulate synaptic plasticity in the perforant pathways of the hippocampus