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  • Alzheimer's Association 24/7 Helpline 800-272-3900 24 hours a day, 365 days a year Free, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
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  • Alzheimer's Foundation of America (AFA) Helpline 866-232-8484 9:00 am - 9:00 pm ET, seven days a week Licensed social workers providing support, info and referrals. Also text message and web chat. Text: 646-586-5283

In a medical emergency, call 911. More numbers, and what each line does, on the help page.

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. Dopamine neuronal loss contributes to memory and reward dysfunction in a model of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Nature communications 2017-04-03 Disease mechanisms

    Alterations of the dopaminergic (DAergic) system are frequently reported in Alzheimer's disease (AD) patients and are commonly linked to cognitive and non-cognitive symptoms.

  2. Memory retrieval by activating engram cells in mouse models of early Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Nature 2016-03-16 Disease mechanisms

    Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive memory decline and subsequent loss of broader cognitive functions.

  3. Cleavage of tau by asparagine endopeptidase mediates the neurofibrillary pathology in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Nature medicine 2014-10-19 Disease mechanisms

    Neurofibrillary tangles (NFTs), composed of truncated and hyperphosphorylated tau, are a common feature of numerous aging-related neurodegenerative diseases, including Alzheimer's disease (AD).

  4. Amyloid-beta (Aβ) D7H mutation increases oligomeric Aβ42 and alters properties of Aβ-zinc/copper assemblies

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. PloS one 2012-04-30 Biomarkers

    Amyloid precursor protein (APP) mutations associated with familial Alzheimer's disease (AD) usually lead to increases in amyloid β-protein (Aβ) levels or aggregation.

  5. Cellular prion protein mediates impairment of synaptic plasticity by amyloid-beta oligomers

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Nature 2009-02-01 Disease mechanisms

    A pathological hallmark of Alzheimer's disease is an accumulation of insoluble plaque containing the amyloid-beta peptide of 40-42 amino acid residues.

  6. Proteomic characterization of postmortem amyloid plaques isolated by laser capture microdissection

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. The Journal of biological chemistry 2004-06-25 Genetics

    The presence of amyloid plaques in the brain is one of the pathological hallmarks of Alzheimer's disease (AD).

  7. Mutations in the beta-amyloid precursor protein are strongly associated with some cases of familial Alzheimer's disease.

  8. The evolving landscape of Alzheimer's disease therapy: From Aβ to tau

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Cell 2025-12-24 Drug development

    A marked evolution in Alzheimer's disease (AD) therapy research is ongoing.

  9. Nanobody Therapeutics in Alzheimer's Disease: From Molecular Mechanisms to Translational Approaches

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Antibodies (Basel, Switzerland) 2025-12-19 Drug development

    Nanobodies (single-domain antibodies, VHHs) have emerged as versatile tools for evaluating and treating Alzheimer's disease (AD).

  10. Senescence in Aging and Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Aging and disease 2025-11-25 Disease mechanisms

    Cellular senescence, once considered a protective mechanism against oncogenesis, is now recognized as a key driver of aging and age-related diseases, including Alzheimer's disease (AD).

  11. Rethinking neurodegeneration through a co-proteinopathy lens

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Trends in neurosciences 2025-11-06 Brain tissue and pathology

    Neurodegenerative diseases have long been considered distinct proteinopathies: amyloid-β and tau in Alzheimer's disease, α-synuclein in Parkinson's disease, and TDP-43 in amyotrophic lateral sclerosis.

  12. TDP-43-proteinopathy at the crossroads of tauopathy: on copathology and current and prospective biomarkers

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Frontiers in cellular neuroscience 2025-10-28 Brain tissue and pathology

    Though usually described as isolated models, neurodegenerative diseases exist in a significant proportion of cases as mixed pathologies, particularly in older adults.

  13. Protein misfolding and its dual role in neurodegeneration and cancer progression

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Advances in protein chemistry and structural biology 2025-10-26 Disease mechanisms

    Protein misfolding is a fundamental biological process with profound implications for human health and disease.

  14. Hyperactive 20S proteasome enhances proteostasis and ERAD in C. elegans via degradation of intrinsically disordered proteins

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Science advances 2025-10-10 Disease mechanisms

    Age-related proteinopathies, including Alzheimer's and Parkinson's disease, are driven by toxic accumulation of misfolded and intrinsically disordered proteins (IDPs) that overwhelm cellular proteostasis.

  15. IRF1 ameliorates synaptic dysfunction through the modulation of O-GlcNAcylation on GluN1 subunit of NMDAR

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Alzheimer's research & therapy 2025-09-30 Disease mechanisms

    In the present study, we demonstrate that Interferon Regulatory Factor-1 (IRF-1), which is deficient in the brain of individuals with Alzheimer's disease (AD), negatively regulates the O-GlcNAcylation levels of GluN1 through transcriptional regulation of the human OGA gene.

  16. Impaired Synaptic Plasticity Mechanisms in Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Metabolic brain disease 2025-09-29 Disease mechanisms

    Alzheimer's disease (AD) is the most common form of dementia, characterized by progressive cognitive decline driven by a complex interplay of genetic, environmental, and lifestyle factors.

  17. Alzheimer's Disease: From Molecular Mechanisms to Promising Therapeutic Strategies

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. International journal of molecular sciences 2025-09-26 Disease mechanisms

    Alzheimer's disease (AD) is the most common cause of dementia worldwide, and there are still no strategies to slow or prevent its clinical progression.

  18. RNF168 dephosphorylation ameliorates cognitive decline in Aβ-based mouse models of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Acta neuropathologica communications 2025-09-24 Disease mechanisms

    Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder among the elderly, with limited effective treatments available in clinical practice.

  19. From Bench to Bedside: Cutting-Edge and Emerging Therapies for Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Central nervous system agents in medicinal chemistry 2025-09-22 Treatments

    Alzheimer's disease (AD) remains one of the most pressing neurodegenerative disorders worldwide, with increasing prevalence and limited disease-modifying treatments.

  20. Understanding Tau pathology: Insights from animal models

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Zoological research 2025-09-18 Drug development

    Tauopathies represent a class of neurodegenerative diseases (NDs), including Alzheimer's disease (AD), progressive supranuclear palsy (PSP), Pick's disease (PiD), and corticobasal degeneration (CBD), defined by intracellular accumulation of misfolded and hyperphosphorylated tau protein.

  21. The tale of donanemab: God is in the details

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Journal of Alzheimer's disease : JAD 2025-09-03 Treatments

    Alzheimer's disease is a major cause of dementia, that affects approximately 7-8% of people aged 65 years and older (according to WHO & Alzheimer's Disease International) and thus is a major concern in public health world-wide.

  22. Optineurin deficiency disrupts phosphorylated tau proteostasis and clusterin expression in human neurons

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Acta neuropathologica communications 2025-09-02 Disease mechanisms

    Optineurin (OPTN) is an autophagy adaptor protein involved in selective autophagy, including aggrephagy and mitophagy.

  23. Role of Monoclonal Antibodies in Alzheimer's Disease: Successes, Failures, and Future Directions

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology 2025-08-30 Treatments

    Alzheimer's disease (AD), referred to as a type of dementia, is a progressive neurodegenerative disease with cognitive decline and key features comprising extracellular amyloid-β(Aβ) and intracellular neurofibrillary tangles.

  24. GLP-1 receptor agonist semaglutide ameliorates motor deficits and tau pathology in the rTg4510s mouse model

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Neuropharmacology 2025-08-27 Drug development

    Semaglutide significantly improved motor coordination in rTg4510 mice on the pole test, though not rotarod endurance.

  25. SENP6 Maintains Mitochondrial Homeostasis by Regulating Mitochondrial Protein Import Through deSUMOylation of TOM40

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 2025-07-29 Disease mechanisms

    SUMOylation, a reversible post-translational modification, regulates various mitochondrial processes, including biogenesis, dynamics, mitophagy, and the mitochondrial unfolded protein response.

From across this topic

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