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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Autophagy and apoptosis are basic physiologic processes contributing to the maintenance of cellular homeostasis.
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Age-related cognitive decline is accompanied by an increase of neuronal apoptosis and a dysregulation of neuroplasticity-related molecules such as brain-derived neurotrophic factor and neurotoxic factors including beta amyloid (Aβ) peptide.
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Psychotic symptoms, delusions and hallucinations, occur in approximately 50% of individuals with Alzheimer's disease (AD) (AD with psychosis [AD + P]).
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Tau aggregation occurs in neurodegenerative diseases including Alzheimer's disease and many other disorders collectively termed tauopathies. trans-cellular propagation of tau pathology, mediated by extracellular tau aggregates, may underlie pathogenesis of these conditions.
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Soluble amyloid-β oligomers (Aβo) trigger Alzheimer's disease (AD) pathophysiology and bind with high affinity to cellular prion protein (PrP(C)).
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(18)F-labeled THK-5105 and THK-5117 are promising candidates as PET tau imaging radiotracers.
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Tau, a microtubule-associated protein, is implicated in the pathogenesis of Alzheimer's Disease (AD) in regard to both neurofibrillary tangle formation and neuronal network hyperexcitability.
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Many neurodegenerative diseases are characterized by the accumulation of insoluble protein aggregates, including neurofibrillary tangles comprised of tau in Alzheimer's disease and Lewy bodies composed of α-synuclein in Parkinson's disease.
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Amyloid β (Aβ) peptides are a primary component of fibrils and oligomers implicated in the etiology of Alzheimer's disease (AD).
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36/100
Synaptic loss is the cardinal feature linking neuropathology to cognitive decline in Alzheimer's disease (AD).
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36/100
The top-down approach to proteomics offers compelling advantages due to the potential to provide complete characterization of protein sequence and post-translational modifications.
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Extensive neuropathological studies have established a compelling link between abnormalities in structure and function of subcortical monoaminergic (MA-ergic) systems and the pathophysiology of Alzheimer's disease (AD).
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In addition to intellectual disability, individuals with Down syndrome (DS) exhibit dementia by the third or fourth decade of life, due to the early onset of neuropathological changes typical of Alzheimer's disease (AD).
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Alzheimer's disease (AD) is a devastating neurodegenerative disorder and the most common cause of elderly dementia.
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The "amyloid-β (Aβ) hypothesis" posits that accumulating Aβ peptides (Aβs) produced by neurons cause Alzheimer's disease (AD).
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DS is the most frequent genetic cause of intellectual disability characterized by the anomalous presence of three copies of chromosome 21.
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Soluble Aβ oligomers are now widely recognized as key pathogenic structures in Alzheimer's disease.
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The variant was not observed in public databases or identified in unrelated subjects.
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Oligomeric forms of amyloid-β peptide (Aβ) are thought to play a pivotal role in the pathogenesis of Alzheimer's disease (AD), but the mechanism involved is still unclear.
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Wnt/β-catenin signalling plays essential roles in embryonic development as well as tissue homoeostasis in adults.
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Glial cell-derived neurotrophic factor (GDNF), and the neurotrophin nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) are important for the survival, maintenance and regeneration of specific neuronal populations in the adult brain.
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The aim of this study was to investigate the effect of liraglutide on Alzheimer-like learning and memory impairment in mice, which were intracerebroventricularly (i.c.v.) injected with streptozotocin (STZ).
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Alzheimer disease is the most prevalent form of dementia globally and is characterized premortem by a gradual memory loss and deterioration of higher cognitive functions and postmortem by neuritic plaques containing amyloid ß peptide and neurofibrillary tangles containing phospho-tau protein.
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Glycogen synthase kinase 3 (GSK3) is a ubiquitously expressed serine/threonine kinase that plays a key role in the pathogenesis of Alzheimer's disease (AD).
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Macroautophagy is an important route in cellular maintenance, in the breakdown and reuse of intracellular materials.
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.
- Reduced phosphatases and hyperphosphorylated glutamatergic receptors persist from early to late stages of prion disease
- Calcium Hypothesis of Alzheimer's disease and brain aging: A framework for integrating new evidence into a comprehensive theory of pathogenesis
- Tau blocks traffic of organelles, neurofilaments, and APP vesicles in neurons and enhances oxidative stress
- The metallobiology of Alzheimer's disease
- Targeting γ-Secretase for Familial Alzheimer's Disease
- Emerging drugs for progressive supranuclear palsy
- Role of Monoclonal Antibodies in Alzheimer's Disease: Successes, Failures, and Future Directions
- Fungally Derived Isoquinoline Demonstrates Inducer-Specific Tau Aggregation Inhibition
- Amyloid beta: structure, biology and structure-based therapeutic development
- LRP/amyloid beta-peptide interaction mediates differential brain efflux of Abeta isoforms