Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Download bibliography of all 1,352 studies, highest score first: BibTeX (.bib) · RIS (.ris)
Highest usefulness score first. Studies without a score come last.
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Immunotherapies targeting extracellular tau share the premise that interrupting cell-to-cell spread of tau pathology in Alzheimer's disease (AD) will slow dementia pathogenesis.
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Phosphorylation renders the PRD significantly resistant to cleavage by the lysosome, especially at less acidic pH setpoints.
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In Alzheimer's disease, tau pathology spreads across brain regions as the disease progresses.
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In the present study, we found senescent aVICs exhibited impaired macroautophagy/autophagy as evidenced by compromised autophagy flux and immature autophagosomes.
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Aging leads to progressive decline in organ and tissue integrity and function, partly due to loss of proteostasis and autophagy malfunctioning.
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Rare mutations in the gene encoding presenilin2 (PSEN2) are known to cause familial Alzheimer's disease (FAD).
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Unlike other aggregation inhibitors, RI-AG03 effectively suppresses aggregation of multiple Tau species containing both hotspots in vitro and in vivo, is non-toxic, and suppresses aggregation-dependent neurodegenerative and behavioral phenotypes.
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Positron Emission Tomography (PET) ligands have advanced Alzheimer's disease (AD) diagnosis and treatment.
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TREM2 trimers remained stably bound, driven primarily by salt bridge between residues D87 and R76 at the interface of TREM2 units.
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46/100
TAR DNA-binding protein 43 (TDP-43) is an RNA binding protein found within ribonucleoprotein granules tethered to lysosomes via annexin A11.
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In APPL/S mice, BD10-2 treatment improved memory and LTP deficits.
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Monoclonal antibodies have emerged as a leading therapeutic agent for the treatment of disease, including Alzheimer's disease.
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Neurons with lower basal UPS activity were more vulnerable to tau accumulation following mild UPS inhibition.
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We and others have shown that [18F]-Flortaucipir, the most validated tau PET tracer thus far, binds with strong affinity to tau aggregates in Alzheimer's (AD) but has relatively low affinity for tau aggregates in non-AD tauopathies and exhibits off-target binding to neuromelanin- and melanin-containing cells, and to hemorrhages.
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Presenilin-2 (PSEN2) mutation Thr421Met was identified from a 57-years old patient with early onset Alzheimer's disease (EOAD) for the first time in Korea.
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Early-onset Alzheimer’s disease (EOAD) is characterized by the presence of neurological symptoms in patients with Alzheimer’s disease (AD) before 65 years of age.
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As an established treatment for movement disorders, deep brain stimulation (DBS) has been adapted for the treatment of Alzheimer's disease (AD) by modulating fornix activity.
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The clinical diagnosis of Creutzfeldt-Jakob disease (CJD) can be supported by several biochemical markers in cerebrospinal fluid (CSF) such as 14-3-3 proteins and tau protein.
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The authors describe a novel missense mutation in the presenilin 2 (PSEN2) gene at residue 439 that predicts an aspartate-to-alanine substitution (D439A).
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45/100
Synaptic dysfunction is a major driver of cognitive decline in Alzheimer's disease (AD), yet its extent and molecular basis in the retina remain poorly defined.
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Alzheimer's disease (AD) is a neurodegenerative disorder characterised by progressive dementia, brain atrophy, and ultimately death.
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45/100
The aggregation of the 42-residue form of the amyloid-β peptide (Aβ42) is important in Alzheimer's disease (AD).
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Autophagy preserves neuronal integrity by clearing damaged proteins and organelles, but its efficiency declines with aging and neurodegeneration.
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Alzheimer's disease (AD) impacts more than half a million people worldwide, with no cure available.
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The emerging class of bispecific antibodies represents a significant advancement in Alzheimer's disease (AD) immunotherapy by addressing the limited brain concentrations achieved with conventional monoclonal antibodies.
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.
- Mutations in the transmembrane domain of APP altering gamma-secretase specificity
- Comparison of Abeta levels in the brain of familial and sporadic Alzheimer's disease
- Amyloid fibril polymorphism: a challenge for molecular imaging and therapy
- Cofilin Suppresses Tau-Induced Defects in Dense-Core Granule Formation and Aβ-Induced Neurodegeneration
- Positively Charged Polyprodrug Amphiphiles with Enhanced Drug Loading and Reactive Oxygen Species-Responsive Release Ability for Traceable Synergistic Therapy
- In silico design and physicochemical characterisation of a dual-action intranasal nanoparticle formulation for Alzheimer’s disease
- DYRK1A, a Dosage-Sensitive Gene Involved in Neurodevelopmental Disorders, Is a Target for Drug Development in Down Syndrome
- Opposing Regulation of Tau Condensation by Phosphorylation Levels and Molecular Chaperone Interactions
- Redox modulation by S-nitrosylation contributes to protein misfolding, mitochondrial dynamics, and neuronal synaptic damage in neurodegenerative diseases
- Brains with sporadic Creutzfeldt-Jakob disease and copathology showed a prolonged end-stage of disease