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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This review summarizes and describes the use of curcumin in diagnosis, prevention, and treatment of Alzheimer's disease.
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The production parameters were optimized by design of experiments.
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Frontotemporal dementia (FTD) is the most common neurodegenerative disorder in individuals under age 60 and has no treatment or cure.
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The accumulation of misfolded α-synuclein (aSyn) and neuron loss define several neurodegenerative disorders including Parkinson's disease (PD) and dementia with Lewy bodies (DLB).
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In Alzheimer's disease, neurofibrillary tangle pathology appears to spread along neuronal connections, proposed to be mediated by the release and uptake of abnormal, disease-specific forms of microtubule-binding protein tau MAPT.
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These findings indicate that AD p-Tau-injected 3 × Tg-AD mice represent a practical model to study the seeding and spread of Tau pathology, their effect on Aβ pathology, and the effect of Tau immunotherapy on both Tau and Aβ pathologies.
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Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the presence in the brain of extracellular amyloid-β protein (Aβ) and intracellular neurofibrillary tangles composed of hyperphosphorylated tau protein.
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The amyloid-β oligomer (AβO) hypothesis was introduced in 1998.
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Decades of research indicate mitochondria from Alzheimer's disease (AD) patients differ from those of non-AD individuals.
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Ensuring cellular protein homeostasis, or proteostasis, requires precise control of protein synthesis, folding, conformational maintenance, and degradation.
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Basal forebrain cholinergic neurons (BFCNs) are believed to be one of the first cell types to be affected in all forms of AD, and their dysfunction is clinically correlated with impaired short-term memory formation and retrieval.
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Oxidative stress is known to play an important role in the pathogenesis of a number of diseases.
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The majority of putative disease-modifying treatments in development for Alzheimer's disease are directed against the amyloid-β (Aβ) peptide.
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Animal models of human diseases that accurately recapitulate clinical pathology are indispensable for understanding molecular mechanisms and advancing preclinical studies.
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Progressive supranuclear palsy (PSP), previously believed to be a common cause of atypical parkinsonism, is now recognised as a range of motor and behavioural syndromes that are associated with a characteristic 4-repeat tau neuropathology.
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We found that brain YKL-40 immunoreactivity was observed in a subset of astrocytes in all four diseases and in controls.
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Although tau has been implicated in diverse neurological diseases, its most pathogenic forms remain to be defined.
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The pathological potential of human astroglia in Alzheimer's disease (AD) was analysed in vitro using induced pluripotent stem cell (iPSC) technology.
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Tau acetylation has recently emerged as a dominant post-translational modification (PTM) in Alzheimer's disease (AD) and related tauopathies.
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Parkinson's disease (PD) is the second most important age-related neurodegenerative disorder in developed societies, after Alzheimer's disease, with a prevalence ranging from 41 per 100,000 in the fourth decade of life to over 1900 per 100,000 in people over 80 years of age.
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Abnormal aggregation of tau in the brain is a major contributing factor in various neurodegenerative diseases.
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The aggregation of amyloid-β peptide (Aβ) has been linked to the formation of neuritic plaques, which are pathological hallmarks of Alzheimer's disease (AD).
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Molecular defects in this gene have been causally associated with Kufor-Rakeb syndrome (#606693), an autosomal recessive form of juvenile-onset parkinsonism, and neuronal ceroid lipofuscinosis (#606693), a neurodegenerative disorder characterized by the intracellular accumulation of autofluorescent lipopigments.
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These findings suggest the potential of passive immunization targeting proximal N-terminal domain tau 6-18 as a disease-modifying approach to AD and related tauopathies.
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This article updates the Calcium Hypothesis of Alzheimer's disease and brain aging on the basis of emerging evidence since 1994 (The present article, with the subtitle "New evidence for a central role of Ca 2+ in neurodegeneration," includes three appendices that provide context and further explanations for the rationale for the revisions in the updated hypothesis-the three appendices are as follows: Appendix I "Emerging concepts on potential pathogenic roles of [Ca 2+ ]," Appendix II "Future studies to validate the central role of dysregulated [Ca 2+ ] in neurodegeneration," and Appendix III "Epilogue: towards a comprehensive hypothesis.")
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.
- Modified Glutamatergic Postsynapse in Neurodegenerative Disorders
- Insight into the kinetic of amyloid beta (1-42) peptide self-aggregation: elucidation of inhibitors' mechanism of action
- Distinct systemic impacts of Aβ42 and Tau revealed by whole-organism snRNA-seq
- Structural Basis for Chaperone-Independent Ubiquitination of Tau Protein by Its E3 Ligase CHIP
- Amelioration of Alzheimer's disease pathology by mitophagy inducers identified via machine learning and a cross-species workflow
- 100 years of Lewy pathology
- TRIM32 Deficiency Impairs Synaptic Plasticity by Excitatory-Inhibitory Imbalance via Notch Pathway
- DSCR1, overexpressed in Down syndrome, is an inhibitor of calcineurin-mediated signaling pathways
- Oligomeric Aβ-induced synaptic dysfunction in Alzheimer's disease
- A4 protein in Alzheimer's disease: primary and secondary cellular events in extracellular amyloid deposition