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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.

  1. Tau proteotasis in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Advances in protein chemistry and structural biology 2024-10-02 Disease mechanisms

    Tau protein accumulation is one of the characteristic features of Alzheimer's disease (AD).

  2. [Anti-Amyloid Antibody Therapy for Alzheimer's Disease]

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Brain and nerve = Shinkei kenkyu no shinpo 2024-10 Treatments

    Alzheimer's disease (AD) is pathologically characterized by deposition of amyloid plaques (comprising amyloid β [Aβ] protein) and neurofibrillary tangles (comprising tau protein), and neuronal death.

  3. Glutamate Transporter 1 as a Novel Negative Regulator of Amyloid β

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Cells 2024-09-24 Biomarkers

    Glutamate transporter-1 (GLT-1) dynamics are implicated in excitotoxicity and Alzheimer's disease (AD) progression.

  4. Transport of β-amyloid from brain to eye causes retinal degeneration in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. The Journal of experimental medicine 2024-09-24 Brain scans and imaging

    The eye is closely connected to the brain, providing a unique window to detect pathological changes in the brain.

  5. NLRP3 inflammasome activation and pyroptosis are dispensable for tau pathology

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Frontiers in aging neuroscience 2024-09-24 Inflammation and the immune system

    Activation of the NLRP3 pathway was observed in the mouse organotypic slice culture (OSC) model following stimulation with LPS and nigericin or exposure to tau seeds.

  6. Amyloid-β Causes NMDA Receptor Dysfunction and Dendritic Spine Loss through mGluR1 and AKAP150-Anchored Calcineurin Signaling

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2024-09-11 Disease mechanisms

    Neuronal excitatory synapses are primarily located on small dendritic protrusions called spines.

  7. Mitigation of synaptic and memory impairments via F-actin stabilization in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Alzheimer's research & therapy 2024-09-07 Disease mechanisms

    We found a significant reduction in PSD-95-actin association in synaptosomes from middle-aged APP/PS1 mice compared to wild-type (WT) mice.

  8. Gut-induced alpha-Synuclein and Tau propagation initiate Parkinson's and Alzheimer's disease co-pathology and behavior impairments

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Neuron 2024-09-05 Brain tissue and pathology

    Tau interacts with α-Synuclein (α-Syn) and co-localizes with it in the Lewy bodies, influencing α-Syn pathology in Parkinson's disease (PD).

  9. [Disease-modifying Drugs for non-Alzheimer Dementias]

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Brain and nerve = Shinkei kenkyu no shinpo 2024-09 Brain tissue and pathology

    Neurodegenerative diseases represent the most common cause of dementia.

  10. Proteostasis disruption and senescence in Alzheimer's disease pathways to neurodegeneration

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Brain research 2024-08-30 Disease mechanisms

    Alzheimer's Disease (AD) is a progressive neurological disease associated with behavioral abnormalities, memory loss, and cognitive impairment that cause major causes of dementia in the elderly.

  11. HLH-30/TFEB modulates autophagy to improve proteostasis in Aβ transgenic Caenorhabditis elegans

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Frontiers in pharmacology 2024-08-30 Disease mechanisms

    Alzheimer's disease (AD) is a complex neurodegenerative disease that affects elderly individuals, characterized by senile plaques formed by extracellular amyloid beta (Aβ).

  12. Cortical neurodegeneration caused by Psen1 mutations is independent of Aβ

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2024-08-13 Risk genes beyond APOE

    Mutations in the PSEN genes are the major cause of familial Alzheimer's disease, and presenilin (PS) is the catalytic subunit of γ-secretase, which cleaves type I transmembrane proteins, including the amyloid precursor protein (APP) to release Aβ peptides.

  13. Alzheimer's disease and sleep disorders: A bidirectional relationship

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Neuroscience 2024-08-11 Risk factors

    Alzheimer's disease (AD) is the most prevalent dementia, pathologically featuring abnormal accumulation of amyloid-β (Aβ) and hyperphosphorylated tau, while sleep, divided into rapid eye movement sleep (REM) and nonrapid eye movement sleep (NREM), plays a key role in consolidating social and spatial memory.

  14. Repurposing Anidulafungin for Alzheimer's Disease via Fragment-Based Drug Discovery

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. ACS chemical neuroscience 2024-08-03 Drug development

    The misfolding and aggregation of beta-amyloid (Aβ) peptides have been implicated as key pathogenic events in the early stages of Alzheimer's disease (AD).

  15. Cholesterol imbalance and neurotransmission defects in neurodegeneration

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Experimental & molecular medicine 2024-08-01 Disease mechanisms

    The brain contains the highest concentration of cholesterol in the human body, which emphasizes the importance of cholesterol in brain physiology.

  16. CCDC50 mediates the clearance of protein aggregates to prevent cellular proteotoxicity

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Autophagy 2024-07-30 Disease mechanisms

    Protein aggregation caused by the disruption of proteostasis will lead to cellular cytotoxicity and even cell death, which is implicated in multiple neurodegenerative diseases.

  17. Endoplasmic reticulum unfolded protein response transcriptional targets of XBP-1s mediate rescue from tauopathy

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Communications biology 2024-07-25 Disease mechanisms

    Pathological tau disrupts protein homeostasis (proteostasis) within neurons in Alzheimer's disease (AD) and related disorders.

  18. Nasal tau immunotherapy clears intracellular tau pathology and improves cognitive functions in aged tauopathy mice

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Science translational medicine 2024-07-03 Drug development

    Pathological tau aggregates cause cognitive decline in neurodegenerative tauopathies, including Alzheimer's disease (AD).

  19. Anti-acetylated-tau immunotherapy is neuroprotective in tauopathy and brain injury

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Molecular neurodegeneration 2024-06-24 Drug development

    Anti-ac-tauK174 treatment mitigates neurobehavioral impairment and reduces tau pathology in PS19 mice.

  20. Tau-targeting nanoparticles for treatment of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Exploration (Beijing, China) 2024-06-21 Drug development

    Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the loss of neural connections and decreased brain tissue volume.

  21. Tau fibrils evade autophagy by excessive p62 coating and TAX1BP1 exclusion

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Science advances 2024-06-12 Disease mechanisms

    The accumulation of protein aggregates is a hallmark of many diseases, including Alzheimer's disease.

  22. Neuronal glutathione depletion elevates the Aβ42/Aβ40 ratio and tau aggregation in Alzheimer's disease mice

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. FEBS letters 2024-05-24 Biomarkers

    Alzheimer's disease (AD) involves reduced glutathione levels, causing oxidative stress and contributing to neuronal cell death.

  23. Diaminocyclopentane - l-Lysine Adducts: Potent and selective inhibitors of human O-GlcNAcase

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Bioorganic chemistry 2024-05-18 Drug development

    A new class of compounds, namely highly substituted diaminocyclopentane-l-lysine adducts, have been discovered as potent inhibitors of O-GlcNAcase, an enzyme crucial for protein de-O-glycosylation.

  24. Alzheimer-like behavior and synaptic dysfunction in 3 × Tg-AD mice are reversed with calcineurin inhibition

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Experimental brain research 2024-05-08 Disease mechanisms

    Alzheimer's disease is a progressive neurodegenerative disorder characterized by impairments in synaptic plasticity and cognitive performance.

  25. Proteostasis in neurodegenerative diseases

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Advances in clinical chemistry 2024-04-30 Disease mechanisms

    Proteostasis is essential for normal function of proteins and vital for cellular health and survival.

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.

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