Get help now — free helplines

You can call any of these for free. You do not need a diagnosis, an appointment, or a crisis to call — questions and plain exhaustion are reasons enough.

  • 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.
  • 988 Suicide & Crisis Lifeline 988 24/7 Call or text 988, or chat at 988lifeline.org. For anyone in emotional distress or a mental-health crisis, including caregivers.
  • 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. Large-scale single-molecule analysis of tau proteoforms

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Nature methods 2025-06-27 Drug development

    Proteins exist as diverse proteoforms resulting from a combination of genetic variation, alternative splicing, and post-translational modifications.

  2. Updates on Tau-Related Drug Targets and Potential Disease-Modifying Therapies for Alzheimer Disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. The American journal of pathology 2025-06-19 TREM2 and immune genetics

    Alzheimer disease (AD) is a chronic, multifactorial neurodegenerative disease affecting a large proportion of the elderly population with detrimental psychological and socioeconomic impacts.

  3. Autophagy and Alzheimer's Disease: Mechanisms and Impact Beyond the Brain

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Cells 2025-06-16 Disease mechanisms

    Alzheimer's disease (AD) is a progressive neurodegenerative disorder marked by neuronal loss, cognitive decline, and pathological hallmarks such as amyloid-beta (Aβ) plaques and tau neurofibrillary tangles.

  4. Chimeric antigen receptors discriminate between tau and distinct amyloid-beta species

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Journal of translational medicine 2025-05-30 Treatments

    DO11.10 cells expressing E2814-CAR-but not Lec-CAR-responded to tau PFFs.

  5. Cell-death pathways and tau-associated neuronal vulnerability in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Cell reports 2025-05-29 Genetics

    Neuronal loss is the ultimate driver of neural system dysfunction in Alzheimer's disease (AD).

  6. Physical exercise mitigates the cognitive impairments by promoting ER-phagy in mice model of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Behavioural brain research 2025-05-23 Disease mechanisms

    Alzheimer's disease (AD) is the primary cause of dementia in older individuals, exhibiting an increasing incidence worldwide.

  7. Distinct systemic impacts of Aβ42 and Tau revealed by whole-organism snRNA-seq

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Neuron 2025-05-16 Genetics

    Both neuronal and peripheral tissues become disrupted in Alzheimer's disease (AD).

  8. Tau aggregation induces cell death in iPSC-derived neurons

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Aging brain 2025-04-11 Drug development

    Abnormal accumulation of tau proteins in the brain is a hallmark of neurodegenerative diseases such as Alzheimer's disease and is closely linked with neuronal cell death.

  9. SFRP1 upregulation causes hippocampal synaptic dysfunction and memory impairment

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Cell reports 2025-04-07 Disease mechanisms

    Impaired neuronal and synaptic function are hallmarks of early Alzheimer's disease (AD), preceding other neuropathological traits and cognitive decline.

  10. Chiral Bimetallic Pt@Au Octapods with Spiral Four-Petal Flower-Like Symmetric Configuration as Sensitive SERS Probes

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Angewandte Chemie (International ed. in English) 2025-03-07 Biomarkers

    Here, we synthesized chiral bimetallic Pt@Au octapods by using l/d-cysteine-threonine (CT) dipeptide as chiral ligands.

  11. Amyloid-β can activate JNK signalling via WNT5A-ROR2 to reduce synapse formation in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Journal of cell science 2025-02-05 Biomarkers

    Wnt signalling is an essential signalling system in neurogenesis, with a crucial role in synaptic plasticity and neuronal survival, processes that are disrupted in Alzheimer's disease (AD).

  12. Tau oligomers impair memory and synaptic plasticity through the cellular prion protein

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Acta neuropathologica communications 2025-01-27 Disease mechanisms

    Deposition of abnormally phosphorylated tau aggregates is a central event leading to neuronal dysfunction and death in Alzheimer's disease (AD) and other tauopathies.

  13. Multi-Targeting Phytochemicals for Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Phytotherapy research : PTR 2025-01-15 Treatments

    Alzheimer's disease (AD) is a type of neurodegenerative illness in which β-amyloid (Aβ) and tau protein accumulate in neurons in the form of tangles.

  14. A Self-Reinforced "Microglia Energy Modulator" for Synergistic Amyloid-β Clearance in Alzheimer's Disease Model

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Angewandte Chemie (International ed. in English) 2025-01-07 Drug development

    Microglial phagocytosis is a highly energy-consuming process that plays critical roles in clearing neurotoxic amyloid-β (Aβ) in Alzheimer's disease (AD).

  15. Targeted demethylation of cathepsin D via epigenome editing rescues pathology in Alzheimer's disease mouse model

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Theranostics 2025-01-01 Biomarkers

    Treatment with Ctsd-targeted dCas9-Tet1 in primary neurons overexpressing mutant APP (mutAPP) reduced Aβ peptide levels and the Aβ42/40 ratio.

  16. Genetically Engineered Mouse Models for Alzheimer Disease and Frontotemporal Dementia: New Insights from Single-Cell and Spatial Transcriptomics

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. The American journal of pathology 2024-12-19 Genetics

    Neurodegenerative diseases, including Alzheimer disease, frontotemporal dementia, Parkinson disease, Huntington disease, and amyotrophic lateral sclerosis, are often casually linked to protein aggregation and inclusion.

  17. Chaperone-mediated autophagy as a modulator of aging and longevity

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Frontiers in aging 2024-12-02 Disease mechanisms

    Chaperone-mediated autophagy (CMA) is the lysosomal degradation of individually selected proteins, independent of vesicle fusion.

  18. Long-term potentiation in the hippocampus: From magnesium to memory

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Neuroscience 2024-11-29 Disease mechanisms

    Long-term potentiation (LTP) is a widely studied phenomenon since the underlying molecular mechanisms are widely believed to be critical for learning and memory and their dysregulation has been implicated in many brain disorders affecting cognitive functions.

  19. Targeting Endogenous Tau in Seeded Tauopathy Models Inhibits Tau Spread

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2024-11-27 Drug development

    The transmission of tau pathology has been proposed as one of the major mechanisms for the spatiotemporal spreading of tau pathology in neurodegenerative diseases.

  20. The Mechanistic Link Between Tau-Driven Proteotoxic Stress and Cellular Senescence in Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. International journal of molecular sciences 2024-11-17 Disease mechanisms

    In Alzheimer's disease (AD), tau dissociates from microtubules (MTs) due to hyperphosphorylation and misfolding.

  21. Decreased lipidated ApoE-receptor interactions confer protection against pathogenicity of ApoE and its lipid cargoes in lysosomes

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Cell 2024-11-11 Genetics

    While apolipoprotein E (APOE) is the strongest genetic modifier for late-onset Alzheimer's disease (LOAD), the molecular mechanisms underlying isoform-dependent risk and the relevance of ApoE-associated lipids remain elusive.

  22. Hyperphosphorylated tau targeting human serum albumin Fusion protein as therapeutics for Alzheimer's diseases

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. IBRO neuroscience reports 2024-11-07 Drug development

    We found that the AL04 treatment decreases hyperphosphorylated tau at PP2A-sensitive epitope Ser202/Thr205 in the hippocampus of the brain.

  23. Molecular Insights into Tau Pathology and its Therapeutic Strategies in Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Journal of integrative neuroscience 2024-10-30 Drug development

    Alzheimer's disease (AD) is the most common cause of dementia.

  24. Repurposing doxycycline for Alzheimer's treatment: Challenges from a nano-based drug delivery perspective

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Brain, behavior, & immunity - health 2024-10-25 Drug development

    Drug repurposing, also known as drug repositioning, involves identifying new applications for drugs whose effects in a disease are already established.

  25. Amyloid pathology and cognitive impairment in hAβ-KI and APPSAA-KI mouse models of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Neurobiology of aging 2024-10-19 Biomarkers

    The hAβ-KI and APPSAA-KI are two amyloid models that harbor mutations in the endogenous mouse App gene.

Other topics