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. Multimodal mediators connecting APOE4 to dementia

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-21 Biomarkers

    We revealed graded, allele dosage‑dependent risk elevations for ACD, AD and VaD among APOE4 carriers, whereby homozygous carriers exhibited substantially higher incident dementia risk relative to heterozygous carriers and non‑carriers across all three clinical endpoints.

  2. Spatial proximity to AD pathology defines cell-type and genotype-specific characteristics in human AD hippocampus

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-21 Genetics

    How amyloid-β (Aβ) plaques and tau phosphorylation spatially relate to cell response and genetic variation in Alzheimer’s disease (AD) brain is currently unclear.

  3. Multi-omics framework prioritizes RNA Methylation Modification Genes in Alzheimer's Disease and Functional Validation of ZFP36 in Regulating Neuroinflammation

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-21 Inflammation and the immune system

    Alzheimer’s disease (AD) is a progressive neurodegenerative disorder, in which epitranscriptomic modifications, especially RNA methylation, may exert crucial regulatory effects.

  4. A brain immune phenotype independent of Alzheimer’s Disease associates with amyloid susceptibility and systemic inflammation

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-21 Brain tissue and pathology

    Transcriptomic and proteomic studies have consistently demonstrated substantial molecular heterogeneity across patients with Alzheimer’s disease (AD) and other neurodegenerative disorders, leading to the proposal of multiple disease subtypes.

  5. Proteomic Signatures of Vulnerability Across Late-Life Depression, Frailty, and Neurodegeneration

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-10-20 Risk factors

    Late-life depression (LLD) is increasingly recognized as a complex multisystem disorder associated with accelerated biological aging, impaired physiological resilience, frailty, and an increased risk of cognitive decline and dementia.

  6. An interpretable whole-blood transcriptomic model for Parkinson’s disease identification and molecular profiling

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-20 Inflammation and the immune system

    ORIGIN-PD enables rational enrichment for NLRP3/NF-κB inhibitor trials by identifying patients with inflammatory involvement.

  7. Coordinated cellular responses track cognitive outcomes in Alzheimer’s disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-20 Brain tissue and pathology

    Individuals with comparable Alzheimer’s disease (AD) pathology can differ markedly in cognition, but the molecular nature of this heterogeneity remains unclear.

  8. Integrating Multisource Target Evidence with Machine-Learning Potency Prediction for Alzheimer’s Disease Drug Discovery

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-20 Digital health tools

    Alzheimer’s disease (AD) target evidence is distributed across biological, chemical, structural, regulatory, and trial-registry sources, complicating reproducible target evaluation and modeling.

  9. Structured Metabolic Genetic Axes Reveal Distinct Lipid and Ketone-Body Programs in Alzheimer’s and Parkinson’s Disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-19 Genetics

    Structured metabolic genetic axes reveal selective and biologically distinct links between circulating metabolism and neurodegenerative disease, providing a framework for mechanism-focused follow-up beyond single-metabolite association.

  10. Sequence-based variant-effect predictions reveal trait-specific regulatory-layer profiles of complex-trait heritability

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-19 Risk factors

    Partitioned-heritability studies have shown which tissues carry the heritability of complex traits, but whether the regulatory layer whose annotations are most informative for heritability within a tissue differs between traits has not been tested, because measured annotations for different layers come from different sets of biosamples.

  11. Spatiotemporal transcriptomic dynamic across the auditory pathway from young to old age in 5xFAD Alzheimer disease mice

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-18 Disease mechanisms

    Auditory dysfunction can precede clinical dementia, but the molecular progression of Alzheimer disease (AD) pathology from the sensory periphery to auditory cortex remains poorly resolved.

  12. Systematic identification of perioperative neurocognitive disorder related biomarkers in Alzheimer’s disease and development of machine learning-based diagnostic models

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-16 Brain tissue and pathology

    Alzheimer’s disease (AD) is a widely prevalent neurodegenerative disorder characterized by progressive cognitive impairment and neuropathological alterations.

  13. Selective vulnerability: validation of atypical neurodegenerative disease variants in histopathological reference cohorts

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-16 Brain tissue and pathology

    Conventional, cohort-based staging exhibited profound topographical inversion, yielding negative correlations for TDP-43 ( ρ = -0.9113, p < 0.001) and α-synuclein ( ρ = -0.8660, p = 0.003) sub-cohorts.

  14. Transcriptomic and phenotypic characterization of Alzheimer’s disease risk genes in neurons and astrocytes highlights shared and cell type specific cellular mechanisms

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-14 Genetics

    Genome-wide association studies have identified nearly 100 genetic loci that affect Alzheimer’s disease risk.

  15. The effects of Arf4 gene knockdown on Alzheimer's amyloid β deposition: Possible role in cognitive resilience

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-14 Risk genes beyond APOE

    Based on the exacerbated AD pathological features and transcriptomic alterations observed in Arf4 knockdown animals, ARF4 appears to play a critical role in AD resilience and may represent a potential prognostic factor worthy of further investigation.

  16. In Vivo Transcriptomics-Based Framework for Systematic Indication Expansion

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-14 Drug development

    Capturing the systemic effects of drugs in vivo remains a fundamental challenge for drug repurposing strategies.

  17. Normative transcriptomic clues to thalamic developmental vulnerability in C9orf7 2-FTLD

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-13 Brain scans and imaging

    This study investigated volumetric MRI differences of the thalamic nuclei in asymptomatic young adult C9orf72 expansion carriers compared to non-carriers, and examined spatial associations with normative thalamic transcriptomics from 8 weeks post-conception through middle age.

  18. Neurodegenerative disorders: Stereotyped relationships between pathological metabolic topographies and the healthy default mode network

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-13 Brain scans and imaging

    The disorders fell into one of three categories based on the topographic relationship of the disease-specific and healthy networks.

  19. Disease-Specific Perturbational Convergence Between Genetic-Risk and Disease-State Transcriptomic Signatures in Alzheimer's Disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-12 Genetics

    In the present analysis, genetic risk and end-stage AD pathology are largely decoupled at the level of individual genes and pathways but converge on a shared, pharmacologically modifiable response landscape.

  20. Surrogate variables and the risk of overfitting in neuropsychiatric gene expression analyses

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-12 Digital health tools

    The reproducibility crisis in biomedical research calls for re-evaluation of how common analytic approaches affect results.

  21. Clinical utility of plasma APOE proteotyping for Alzheimer’s disease risk and prognosis

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-11 Genetics

    Plasma APOE4 proteotyping accurately distinguished genotype-defined APOE ε4 carrier status and copy number while demonstrating AD-related associations comparable to DNA genotyping.

  22. Mapping polygenic risk scores to brain cells: insights for neurodegenerative diseases

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-11 Genetics

    Neurodegenerative diseases (NDDs) are driven by multiple related yet distinct pathological processes that evolve over decades, resulting in substantial clinical and neuropathological heterogeneity.

  23. Expression predictions inform molecular interpretation of Alzheimer’s disease risk loci

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-11 Genetics

    Sequence models predict the molecular effects of genetic variation, yet their contribution to interpreting Alzheimer’s disease (AD) association signals remains uncertain.

  24. Subtype-Selective Neuronal Vulnerability and Compensatory Neuroglial Remodeling in Human Cortical Dementia

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-11 Disease mechanisms

    Whether the nodal vulnerability in dementia is solely represented by changes in cellular abundance or attrition of cellular transcriptomic landscape attribute to that transition in aging brain is yet to uncover with minutiae.

  25. MTHFR*677C>T produces distinct prodromal disease signatures in a mouse model of late-onset Alzheimer’s disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-09 TREM2 and immune genetics

    These data further support the use of the LOAD2.Mthfr 677C>T mouse model to study aspects of ADRD such as cerebrovascular compromise.

From across this topic

10 of the 933 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.

Other topics