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. Integrative single-nucleus multi-omics profiling identifies candidate regulators and signaling axes in Alzheimer’s disease lipid-processing microglia

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-07-14 Drug development

    Lipid-processing microglia are among the microglial states most strongly associated with Alzheimer’s disease (AD) pathology, yet whether this association reproduces across independent cohorts, what transcriptional programs define the state, and which upstream signals and small molecules can modulate it remain unsolved.

  2. EcoXAI: Autonomous Agentic Ecosystem for Explainable Artificial Intelligence and Biomedical Discovery

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-07-13 Drug development

    EcoXAI replaces monolithic AI text interfaces with an autonomous execution-driven framework with specialized bioinformatics agents for delivering proactive, data-driven insights grounded in established biological knowledge.

  3. Longitudinal plasma proteomics separates diagnostic differences from progression-linked changes in Alzheimer’s disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-07-10 Prevention trials

    Most plasma proteomic studies in Alzheimer’s disease (AD) compare cases and controls cross-sectionally, leaving unresolved which AD-associated proteins mark diagnostic states and which are linked to disease progression.

  4. Early Prediction of Parkinson’s Disease Progression by Integrating Research Cohort and Real-World Data Using Knowledge-Anchored Graph Learning

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-07-09 Digital health tools

    Parkinson’s disease (PD) progression is highly heterogeneous.

  5. TrustPGS: When can a polygenic score be trusted? A per-individual reliability framework across ancestries

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-07-07 Clinical trials

    Polygenic scores summarise genetic predisposition to a trait, but a population-level accuracy figure cannot tell a clinician whether a given prediction is reliable for the person in front of them.

  6. Trisomy 21 cerebral organoids exhibit Alzheimer’s disease amyloid and apolipoprotein E co-pathologies

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-07-07 Down syndrome and Alzheimer's

    Adults with Down syndrome (DS) develop Alzheimer’s disease (AD) brain pathology by age 40 due to triplication of the Amyloid Precursor Protein ( APP ) gene on chromosome 21.

  7. Effect of Intensive vs Standard Blood Pressure Control According to APOE ε4 Genotype: A Secondary Analysis of SPRINT

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-07-06 Disparities

    In SPRINT, intensive vs standard SBP control yielded a significantly larger 4-year absolute risk reduction in dementia among APOE ε4 carriers (−1.7%) than non-carriers (0.2%; P-interaction = .045); the relative-scale interactions were directionally consistent but not significant.

  8. HnRNPAB -targeted antisense oligonucleotides ameliorate tau pathology and cognitive deficits by modulating Alzheimer’s disease-associated alternative splicing

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-07-03 Drug development

    Aberrant alternative splicing alters multiple disease-associated splicing events, including MAPT exon 10 inclusion linked to tau pathology, and thereby impacts Alzheimer’s disease (AD) progression.

  9. Age-Related Speech-in-Noise Hearing Loss in Parkinson’s Disease and APOE E4 Carriers

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-06-09 Risk factors

    Age-related hearing loss is a leading modifiable risk factor for dementia and is increasingly recognized as a non-motor feature of Parkinson’s disease (PD).

  10. Biopsychosocial risk factors for Alzheimer’s disease and related dementias in UK immigrants from the Middle East and North Africa (MENA)

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-05-13 Risk factors

    The Middle East and North Africa (MENA) region represents the area of greatest projected growth in instances of Alzheimer’s disease and related dementias (ADRDs) globally, yet, it remains virtually uncharacterized in health studies of aging and ADRDs.

  11. Epigenetically constrained astrocyte states underlie prefrontal cortex vulnerability in Down syndrome–associated Alzheimer’s disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-04-21 Down syndrome and Alzheimer's

    Down syndrome (DS), caused by trisomy 21, confers a near-universal risk for Alzheimer’s disease (AD), yet individuals exhibit marked variability in cognitive decline, suggesting the presence of cellular mechanisms that modulate vulnerability and resilience.

  12. The Amyloid Plaque Proteomes of Alzheimer’s Disease and Mild Cognitive Impairment

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-03-08 Down syndrome and Alzheimer's

    Amyloid plaques contain numerous proteins in addition to amyloid beta in Alzheimer’s disease (AD).

  13. Plasma Proteomic Analysis of APOE ε4 Homozygotes Identifies Preclinical Alzheimer’s Disease Alterations Potentially Modulated by Semaglutide

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-02-17 Drug development

    Individuals who carry two copies of the apolipoprotein E ε4 ( APOE ε4) allele are at high risk of developing Alzheimer’s disease (AD), yet the effects of APOE ε4 homozygosity on biological pathways related to AD over the lifespan are unknown.

  14. Proteomic biomarkers of cognitive function, APOE ε4 status, and dementia in Generation Scotland

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-01-29 Biomarkers

    Untargeted mass spectrometry remains underutilised for blood-based biomarker discovery in dementia research from large cohorts, where affinity-based approaches dominate.

  15. ATN Classification and Machine-Learned Plasma Biomarker Phenotypes Reveal Distinct Alzheimer’s Pathology in a Population-Based Cohort

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-01-06 Biomarkers

    The analytic sample included 4,465 individuals (mean age 69.7±10.4 years; 58.7% female; 75.8% non-Hispanic White).

  16. Genetic drivers of progression in Alzheimer's disease are distinct from disease risk

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv : the preprint server for health sciences 2025-11-19 Genetics

    Established AD risk factors, including APOE ε4 dosage and polygenic risk scores, were not associated with disease progression amyloid positive individuals who are actively declining.

  17. Spatial Multi-Omics Workflow and Analytical Guidelines for Alzheimer's Neuropathology

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv : the preprint server for biology 2025-11-17 Genetics

    Spatial biology technologies enable high-dimensional profiling within intact tissues, revealing how molecular and cellular organization drives function and disease.

  18. Consensus meta-analysis of genome-wide association studies for Alzheimer's disease and related dementia

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv : the preprint server for health sciences 2025-10-23 Genetics

    To better characterize the genetic architecture underlying Alzheimer's disease (AD) and related dementia (ADRD), we performed a meta-analysis of European ancestry genome-wide association studies in 128,681 cases or proxy cases of ADRD and 849,833 (proxy) controls.

  19. Cross-Ancestry Polygenic Risk Scores Enhance Alzheimer's Disease Risk Prediction in Multiethnic Cohorts

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv : the preprint server for health sciences 2025-10-07 Genetics

    The cross-ancestry Bayesian PRS model demonstrated the highest predictive performance in non-European populations.

  20. Brain Region-Specific Epigenomic Reorganization and Altered Cell States in Alzheimer's Disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv : the preprint server for biology 2025-09-30 Genetics

    Alzheimer's disease (AD) is the most common neurodegenerative disorder, yet the molecular mechanisms underlying its region- and cell-type-specific pathogenesis remain poorly defined.

  21. miR155 triplicated in Down syndrome regulates hippocampal GABAergic neurogenesis in Alzheimer’s disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2025-09-30 Down syndrome and Alzheimer's

    MicroRNA dysregulation is implicated in neurodegenerative disorders, including Alzheimer’s disease (AD).

  22. APOE genotypes differentially remodel the astrocytic lipid droplet-associated proteome to shape lipid droplet dynamics

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv : the preprint server for biology 2025-08-20 Genetics

    The lipids and proteins that comprise lipid droplets regulate several cellular functions including lipid storage, stress responses, and inflammation.

  23. Biological Age and Age Acceleration Predict Alzheimer's Disease Plasma Biomarker Levels

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv : the preprint server for health sciences 2025-08-08 Biomarkers

    Epigenetic clocks can predict pathological aging associated with Alzheimer's disease (AD) risk, albeit findings are mixed regarding if clocks are predictive in blood and in non-European populations.

  24. Harnessing the Evolution of Proteostasis Networks to Reverse Cognitive Dysfunction

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2025-03-02 Down syndrome and Alzheimer's

    The integrated stress response (ISR) is a highly conserved network essential for maintaining cellular homeostasis and cognitive function.

  25. Shared Genetic Architecture Between COVID-19 Severity and Alzheimer's Disease Across European and African Ancestries

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research square 2024-12-24 Genetics

    The global outbreak of COVID-19, caused by the SARS-CoV-2 virus, has been linked to long-term neurological complications, including an increased risk of Alzheimer's disease (AD) among older adults.

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