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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Protein conformational diseases, including Alzheimer's, Huntington's, and Parkinson's diseases, result from protein misfolding, giving a distinct fibrillar feature termed amyloid.
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Metastable oligomeric and protofibrillar forms of amyloidogenic proteins have been implicated as on-pathway assembly intermediates in amyloid formation and as the major toxic species in a number of amyloid diseases including Alzheimer's disease.
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Neurofibrillary tangles composed of hyperphosphorylated, aggregated tau are a common pathological feature of tauopathies, including Alzheimer's disease.
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Accumulation of amyloid beta-protein (Abeta) is a fundamental feature of certain human brain disorders such as Alzheimer's disease (AD) and Down syndrome and also of the skeletal muscle disorder inclusion body myositis (IBM).
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Citrullinated proteins are the products of a posttranslational process in which arginine residues undergo modification into citrulline residues when catalyzed by peptidylarginine deiminases (PADs) in a calcium ion-dependent manner.
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Alzheimer's disease (AD) is a progressive neurodegenerative disorder for which there are few therapeutics that affect the underlying disease mechanism.
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Proteins can become modified by a large number of reactions involving reactive oxygen species.
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36/100
Endocytosis is universally important in cell function.
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The accumulation of lysosomes and their hydrolases within neurons is a well-established neuropathologic feature of Alzheimer disease (AD).
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Gene knockout studies in mice suggest that presenilin 1 (PS1) is the major gamma-secretase and that it contributes disproportionately to amyloid beta (Abeta) peptide generation from beta-amyloid precursor protein (APP), whereas PS2 plays a more minor role.
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Conformational diseases are caused by mutations altering the folding pathway or final conformation of a protein.
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Amyloid fibrils are a polymeric form of protein, involving a continuous beta-sheet with the strands perpendicular to the long axis of the fibril.
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Alzheimer's disease (AD) involves amyloid beta (Abeta) accumulation, oxidative damage, and inflammation, and risk is reduced with increased antioxidant and anti-inflammatory consumption.
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Owing to improving preventative, diagnostic, and therapeutic measures for cardiovascular disease and a variety of cancers, the average ages of North Americans and Europeans continue to rise.
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Neurofibrillary tangles (NFT) containing paired helical filaments (PHF) composed of abnormally phosphorylated tau are one of the hallmark lesions of the Alzheimer's disease (AD) brain.
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The salutary intersection of fundamental cell biology with the study of disease is well illustrated by the emerging elucidation of neurodegenerative disorders.
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The cognitive hallmark of early Alzheimer's disease (AD) is an extraordinary inability to form new memories.
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Accumulating evidence points to an important role of intraneuronal A beta as a trigger of the pathological cascade of events leading to neurodegeneration and eventually to Alzheimer's disease (AD) with its typical clinical symptoms, like memory impairment and change in personality.
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The problem with pure recombinant or synthetic antigens used in modern day vaccines is that they are generally far less immunogenic than older style live or killed whole organism vaccines.
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Mechanisms of brain and retinal iron homeostasis have become subjects of increased interest after the discovery of elevated iron levels in brains of patients with Alzheimer's disease and retinas of patients with age-related macular degeneration.
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Treating Alzheimer's disease (AD) is the biggest unmet medical need in neurology.
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Amyloid fibrils are ordered aggregates of peptides or proteins that are fibrillar in structure and contribute to the complications of many diseases (e.g., type 2 diabetes mellitus, Alzheimer's disease, and primary systemic amyloidosis).
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Acutely developing lesions of the brain have been highly instructive in elucidating the neural systems underlying memory in humans and animal models.
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Amyloid beta-peptide (Abeta) is known to induce free radical-mediated oxidative stress in the brain.
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LRP (low-density lipoprotein receptor-related protein) is linked to 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.
- Amyloid beta peptide and NMDA induce ROS from NADPH oxidase and AA release from cytosolic phospholipase A2 in cortical neurons
- Aβ seeding potency peaks in the early stages of cerebral β-amyloidosis
- Lecanemab, Aducanumab, and Gantenerumab - Binding Profiles to Different Forms of Amyloid-Beta Might Explain Efficacy and Side Effects in Clinical Trials for Alzheimer's Disease
- The amyloid state and its association with protein misfolding diseases
- Evaluation of [18F]MK-6240 binding to tau protein in postmortem human brains of Down syndrome and Alzheimer’s disease and assessment of off-target (non-tau) binding
- Proteomic analysis of protein homeostasis and aggregation
- Expanding RNAi therapeutics to extrahepatic tissues with lipophilic conjugates
- RNA Oxidation Is a Prominent Feature of Vulnerable Neurons in Alzheimer’s Disease
- Exercise plays a preventive role against Alzheimer's disease