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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Tauopathies are neurodegenerative diseases characterized by accumulation of Tau amyloids, and include Alzheimer disease and certain frontotemporal dementias.
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Three Newcastle patients bearing an expansion in C9ORF72 were identified.
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Targeting pathological tau protein in Alzheimer's disease (AD) and related tauopathies has shown great potential in animal models.
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36/100
Alzheimer's disease (AD) is the most common form of dementia in individuals over 65 years of age and is characterized by accumulation of beta-amyloid (Aβ) and tau.
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Presenilins play essential roles in memory formation, synaptic function, and neuronal survival.
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In Alzheimer's disease (AD), the pathological accumulation of tau appears to be a downstream effect of amyloid β protein (Aβ).
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Treatment of neurodegenerative disorders such as Alzheimer's disease is hampered by the blood-brain barrier (BBB).
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We found a significantly greater intensity of cytoplasmic immunostaining for HDAC4 and HDAC6 in granule cells of the dentate gyrus in cases of FTLD overall compared with controls, and specifically in cases of FTLD tau‐ P icks compared with FTLD tau‐ MAPT and controls.
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In addition to the deposition of tau oligomers, our results also provide compelling evidence of co-occurrence of α-synuclein and tau into their most toxic forms, i.e., oligomers suggesting that these species interact and influence each other's aggregation via an interface in synucleinopathies.
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Currently available therapies for adult onset neurodegenerative diseases provide symptomatic relief but do not modify disease progression.
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Alzheimer's disease is characterized by the accumulation of amyloid-β (Aβ) and Tau in the brain.
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The concept of molecular mimicry was established to explain commonalities of structure which developed in response to evolutionary pressures.
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Mitochondria form a highly interconnected tubular network throughout the cell via a dynamic process, with mitochondrial segments fusing and breaking apart continuously.
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Circadian rhythms are physiological and behavioural cycles generated by an endogenous biological clock, the suprachiasmatic nucleus.
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The presenilin-containing γ-secretase complex produces the amyloid β-peptide (Aβ) through intramembrane proteolysis, and >100 presenilin mutations are associated with familial early-onset Alzheimer disease (AD).
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Disruption of autophagy plays an import role in neurodegenerative disorders, where deficient elimination of abnormal and toxic protein aggregates promotes cellular stress, failure and death.
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Immunization is increasingly recognized as a suitable therapeutic avenue for the treatment of neurological diseases such as Alzheimer's disease and other tauopathies.
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In sporadic Alzheimer's disease (AD), impaired Aβ removal contributes to elevated extracellular Aβ levels that drive amyloid plaque pathogenesis.
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The phenomenon of protein aggregation and amyloid formation has become the subject of rapidly increasing research activities across a wide range of scientific disciplines.
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The collapse of neural networks important for memory and cognition, including death of neurons and degeneration of synapses, causes the debilitating dementia associated with Alzheimer's disease (AD).
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NMDA receptor (NMDAR)-induced excitotoxicity is thought to contribute to the cell death associated with certain neurodegenerative diseases, stroke, epilepsy, and traumatic brain injury.
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Recent trials of anti-amyloid agents have not produced convincing improvements in clinical outcome in Alzheimer's disease; however, the reason for these poor or inconclusive results remains unclear.
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Several studies have highlighted the frequency of sleep disturbances in Alzheimer's disease (AD).
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Neurodegenerative disease is one of the greatest health crises in the world and as life expectancy rises, the number of people affected will continue to increase.
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Although biotherapeutics have vast potential for treating brain disorders, their use has been limited due to low exposure across the blood-brain barrier (BBB).
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.
- Role of neurotoxicants in the pathogenesis of Alzheimer's disease: a mechanistic insight
- The ubiquitin proteasome system in neurodegenerative diseases: sometimes the chicken, sometimes the egg
- Alzheimer's disease-like pathological features in transgenic mice expressing the APP intracellular domain
- LATE-NC aggravates GVD-mediated necroptosis in Alzheimer's disease
- Nitration of tau protein is linked to neurodegeneration in tauopathies
- Genetics, Functions, and Clinical Impact of Presenilin-1 (PSEN1) Gene
- The therapeutic landscape of tauopathies: challenges and prospects
- TRPMLs and TPCs: Targets for lysosomal storage and neurodegenerative disease therapy?
- Anti-amyloid-β Antibodies and Anti-tau Therapies for Alzheimer's Disease: Recent Advances and Perspectives
- Disrupting SORL1-retromer endosomal recycling in mice drives the age-dependent neurodegenerative signature of Alzheimer's disease