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Newest in this topic

  1. Integrative systems biology identifies shared neuroimmune co-expression programmes across pulmonary tuberculosis and Alzheimer's disease 2026-10-30
  2. Pregnancy History and Loss of Normal PSEN2 Function Impact Female Late-Life Cognitive Processing, Inhibitory Signaling, and Gliosis 2026-10-30
  3. Joint localization and testing reveals spatial context of differential expression 2026-10-29

Studies

274 studies carry this tag.

Date range

1997 to 2026

Top journals

  • bioRxiv 44
  • Research Square 16
  • Nature neuroscience 11
  • Nature communications 10
  • Neuron 10

98 journals in all.

Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.

  1. Integrative systems biology identifies shared neuroimmune co-expression programmes across pulmonary tuberculosis and Alzheimer's disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-30 Genetics

    Active PTB was associated with widespread transcriptional remodeling, with 1,389 dysregulated genes organized into 16 PTB-associated co-expression modules.

  2. Pregnancy History and Loss of Normal PSEN2 Function Impact Female Late-Life Cognitive Processing, Inhibitory Signaling, and Gliosis

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-30 Risk genes beyond APOE

    This work suggests that although parity history and PSEN2 deficiency exert individual differing age-related effects on cognition and neurobiology, they do not act synergistically.

  3. Joint localization and testing reveals spatial context of differential expression

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-29 Genetics

    Multi-subject spatial transcriptomics is increasingly used to identify molecular differences across individuals and conditions while resolving where in tissue those differences occur.

  4. PIN1-p53 bifurcation dictates opposite cell fate decisions in Alzheimer’s disease and glioblastoma via distinct energy landscape topologies

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-29 Genetics

    Although Alzheimer’s disease (AD) and glioblastoma (GBM) share common aging-related risk factors, they lead to opposite cellular fates—neurodegeneration versus uncontrolled proliferation.

  5. Single-Nucleus Profiling Reveals Neuronal Metabolic Collapse During the Transition to Alzheimer’s Disease Dementia

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-28 Genetics

    Current Alzheimer’s disease (AD) neuropathological metrics, including Thal phasing, and Braak staging, often do not accurately predict cognitive status: many cognitively resilient individuals have substantial pathological burdens, whereas some patients with dementia show minimal classical AD pathology.

  6. CEP-IP with CMRF in SEA-AD Microglia: A Mitochondrial Co-expression Module Linked to Cognition

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-27 Genetics

    Single-nucleus RNA-seq (snRNA-seq) studies of Alzheimer’s disease (AD) routinely filter nuclei by mitochondrial percentage (%MT) or remove mitochondrial genes, yet whether these reads carry information about cognition is rarely examined.

  7. CausalDiffChem: Causal Network Restoration for Therapeutic Prioritization and Repurposing Across Diseases

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-26 Genetics

    Computational drug repurposing commonly relies on transcriptomic signature matching to identify compounds that reverse disease-associated gene expression, but such approaches do not distinguish putative causal drivers from downstream consequences of disease.

  8. Proteogenomics captures a midlife biological state of Alzheimer’s disease susceptibility

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-26 Genetics

    Alzheimer’s disease (AD) develops over decades, but biological processes underlying susceptibility during midlife remain poorly understood.

  9. Ultra-sensitive Mapping of Cell-free DNA-derived Methylomes Reveals Brain-specific Epigenetic Alterations Implicated in Alzheimer’s Disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-26 Long-term cohort studies

    DNA cytosine modifications play a crucial role in gene regulation that underlies the pathogenesis of complex diseases such as Alzheimer’s disease (AD).

  10. Non-canonical proteoforms of the human fusiform gyrus in Alzheimer’s disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-25 Genetics

    For a long time, the protein coding potential of our genome was underestimated.

  11. Alzheimer’s Disease-Associated Proteomic Changes in Olfactory Stem Cells Show Pathway-Level Transcriptomic Overlap

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-24 Genetics

    Alzheimer’s disease (AD) is a progressive, neurodegenerative disorder and the leading cause of dementia worldwide.

  12. Overcoming segmentation bottlenecks in brain tissue for spatial proteomic inference at population scale

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-24 Genetics

    In spatial proteomics across large cohorts, downstream estimates from tens of thousands of images depend on accurate cell segmentation.

  13. A coordinated and reproducible multicellular response to AD pathology

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-23 Brain tissue and pathology

    While single-cell measurements of the Alzheimer’s disease (AD) brain allow investigation of vulnerable cells in unprecedented depth, reported findings are heterogeneous, mostly descriptive and often ignore interdependence of cellular responses.

  14. 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.

  15. Function-oriented microglial transcriptional scores in Alzheimer’s disease: resolving terminal functions beyond activation states

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

    Alzheimer’s disease (AD) staging based on amyloid-β, tau, and neurodegeneration does not capture heterogeneous microglial functions.

  16. 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.

  17. 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.

  18. 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.

  19. 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.

  20. Longitudinal single-cell transcriptional profiling identifies dynamic neurodegenerative mechanisms in Christianson Syndrome rat

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-20 Risk genes beyond APOE

    Endolysosomal dysfunction is a central feature of many neurodegenerative disorders.

  21. 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.

  22. Female microglia show heightened responses to aging and amyloid pathology in mice and humans

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-19 Risk genes beyond APOE

    These findings identify conserved regulatory networks that may contribute to female-biased microglial responses to AD pathology across mice and humans.

  23. 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.

  24. 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.

  25. 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.

  26. 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.

  27. These findings demonstrate that Tau deletion induces an active, multilevel gain-of-resilience rather than passive resistance.

  28. 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.

  29. 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.

  30. 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.

  31. 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.

  32. 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.

  33. 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.

  34. Cross-Tissue Inflammatory Convergence Supports a Putative Muscle–Brain Axis in Alzheimer’s Disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-08 Mild cognitive impairment

    Aging muscle showed increased inflammatory, extracellular-matrix, and stromal communication programs.

  35. Triple-Omics Analysis Unveiled the Neuroprotective Mechanisms of Akkermansia muciniphila in an Environmental Exposure-Linked Mouse Model of Alzheimer’s Disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-07 Risk factors

    These findings identify restoration of hippocampal transcript fate and splice-isoform selection as a mechanism potentially underlying A. muciniphila -mediated protection against Cd neurotoxicity, and establish post-transcriptional RNA regulation as a gut-brain target for mitigating environmentally driven neurotoxicity.

  36. Circular Data Analysis for Spatial Omics

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-06 Risk factors

    Many biological quantities in omics are inherently periodic or directional, including circadian phase, cell-cycle position, and cellular orientation.

  37. Cross-Dataset Reanalysis of Mouse Alzheimer Disease Single-Cell RNA-Sequencing Data Reveals a Reproducible Innate Immune Activation Signature

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-06 TREM2 and immune genetics

    Single-cell RNA sequencing (scRNA-seq) studies of Alzheimer’s disease (AD) mouse models have proliferated across independent laboratories, brain regions, and platforms, yet the cross-study reproducibility of transcriptional signatures derived from such data remains underexplored.

  38. Large-scale cerebrospinal fluid proteomics identifies diagnostic biomarker candidates across the clinico-pathological continuum of frontotemporal lobar degeneration

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-05 Tau biomarkers

    Frontotemporal lobar degeneration (FTLD), predominantly comprised of tau and TDP-43 proteinopathies, is a common cause of early-onset dementia.

  39. DNA polymerase kappa supports repair-associated DNA synthesis and neuronal genome resilience

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-04 Risk factors

    Postmitotic neurons must preserve genome integrity for decades despite continuous oxidative, transcription-associated, and environmental DNA damage.

  40. Stage-specific proteomic signatures of synaptopathy in Alzheimer’s disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-03 Disease mechanisms

    Synapse loss is the strongest pathological correlate of cognitive decline in Alzheimer’s disease, yet the molecular basis of synaptic vulnerability across disease progression remains poorly understood.

  41. Integrating CSF and EV Proteomes Enhances Biomarker Discovery by Capturing Shared Variation Across Compartments

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-02 Tau biomarkers

    Cerebrospinal fluid (CSF) contains brain derived proteins that can be leveraged as biomarkers for Alzheimer’s disease (AD) and other neurodegenerative diseases.

  42. Glial Transcriptomic Convergence in Alzheimer’s and Parkinson’s Disease with Independent Retinal and Aqueous-Humor Evidence

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-09-30 Brain scans and imaging

    We then integrated healthy retinal expression, AD retinal proteomics, and PD aqueous-humor proteomics with the brain-concordance results.

  43. Predicting Rates of Cognitive Decline in Older Adults with Brain- and Cardiac-Imputed Transcripts

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-09-30 Drug development

    Severe cognitive decline due to dementia is an important clinical indicator signaling neurodegeneration.

  44. A single-nuclei multiomics resource across four brain regions prioritises human neural cell types influencing brain-related traits

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-25 Genetics

    Genetic studies have identified thousands of variants associated with brain-related traits.

  45. DNA Methylation Concordance Between Fresh-Frozen and Formalin-Fixed Paraffin-Embedded Human Brain Tissue in Neurodegenerative Diseases

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-09-24 Lewy body dementia

    Formalin-fixed, paraffin-embedded (FFPE) brain tissue is a major archival resource, yet its suitability for high-density DNA methylation profiling is limited by fixation-induced DNA fragmentation and crosslinking.

  46. LSD-pipeline: Causal Inference of miRNA Network Effects in Alzheimer's Disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-24 Disease mechanisms

    MicroRNAs (miRNAs) are implicated in Alzheimer's disease (AD), but research has focused on individual miRNAs and direct targets.

  47. High-Dimensional Multi-Omic Mapping of Post-Mortem Human Brain Using Iterative Indirect Immunofluorescence Imaging on Xenium-Processed Tissues

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-23 Digital health tools

    Immunofluorescence staining of FFPE tissue following Xenium processing also preserves cellular morphology, allowing the morphological complexity of distinct cell types to be captured and quantitated, especially for glial cells with highly ramified processes.

  48. A lifespan single-cell atlas of the human developing hippocampus benchmarks familial Alzheimer’s disease brain organoids

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-20 Risk genes beyond APOE

    Familial Alzheimer’s disease (fAD) is an early-onset form of AD caused by autosomal-dominant variants in APP, PSEN1, or PSEN2, with PSEN1 accounting for most genetically defined cases [1].

  49. Loss of TDP-43 function drives cryptic circular RNAs in neurodegenerative diseases

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-20 Lewy body dementia

    TAR DNA-binding protein 43 (TDP-43) is a key pathological hallmark of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) and a critical regulator of RNA splicing.

  50. TDP-43 dysfunction induces cryptic circular RNAs in ALS/FTD

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-20 Genetics

    Nuclear depletion of TDP-43 is a defining pathological feature of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), leading to widespread RNA misprocessing, including the formation of cryptic exons.

From across this tag

9 of the 274 studies in this tag, 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 9. The same 9 appear here every time.

All topic tags with their study counts