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Home › Research › Topic

Brain proteins, microglia and lab models

4,948 studies in this group. A computer grouped them by what their titles and summaries are about, not by a hand-made list. The name describes most of the group, not every study in it.

Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.

Download bibliography of all 4,948 studies, highest score first: BibTeX (.bib) · RIS (.ris)

Highest usefulness score first. Studies without a score come last.

  1. Impaired cerebrovascular-cerebrospinal fluid coupling is associated with non-motor features of Lewy body disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-19 Brain scans and imaging

    Parkinsons disease and dementia with Lewy bodies patients both demonstrated weaker global BOLD-CSF coupling compared to controls, with no detectable difference between patient groups.

    Why it matters

    People with Parkinson's disease and dementia with Lewy bodies showed weaker coordination between cerebrovascular activity and cerebrospinal fluid inflow than controls, and this was linked to hallucinations, cognitive fluctuations and poorer sleep. The authors describe this as preliminary evidence and call for replication in larger cohorts.

  2. GCH1 genetic variation as a prognostic factor in Parkinsons disease across populations

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-19 How common it is

    BackgroundPathogenic variants in GCH1 have been associated with Parkinsons disease (PD), but the clinical phenotype and longitudinal disease course of GCH1-associated PD remain incompletely characterized.

    Why it matters

    Pathogenic or likely pathogenic GCH1 variants were more common in Parkinson's disease patients than controls and were linked to earlier disease onset. This concerns the genetic and clinical features of Parkinson's disease, not Alzheimer's disease treatment, cure or prevention.

  3. Fine-mapping reveals four TMEM106B haplotypes associated with neurodegenerative risk and preserved cognition at extreme age

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-17 Genetics

    Genetic variation at the TMEM106B locus has been associated with Alzheimers disease (AD) and related neurodegenerative phenotypes, yet its haplotypic architecture remains incompletely resolved.

    Why it matters

    Fine-mapping of the TMEM106B locus identified four haplotypes, one of which was strongly enriched in cognitively healthy centenarians. This describes genetic architecture linked to Alzheimer's risk and preserved cognition at extreme age, not a treatment or cure.

  4. A Phase 2b randomized clinical trial of the oral p38α inhibitor neflamapimod in dementia with Lewy bodies (DLB)

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-08-14 Tau biomarkers

    There is high unmet need in dementia with Lewy bodies (DLB).

    Why it matters

    This 16-week randomized placebo-controlled trial with a 32-week open label extension tested the oral p38α inhibitor neflamapimod in 159 people with probable dementia with Lewy bodies, enriched for those without Alzheimer's disease co-pathology. It concerns dementia with Lewy bodies, not Alzheimer's disease, so it does not show a way to treat, cure, or prevent Alzheimer's disease.

  5. Diffusion kurtosis imaging (gen)omics unravels mechanisms of cerebral small vessel disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv (preprint) 2026-08-14 Biomarkers

    Cerebral small vessel disease (cSVD) is a leading cause of stroke and dementia.

    Why it matters

    This genomic and omics study of diffusion kurtosis imaging markers identified genetic loci and genes tied to cerebral small vessel disease, a leading cause of stroke and dementia. It maps biological mechanisms and clinical relevance rather than testing any treatment or prevention.

  6. Population-based reference equations and Z-scores for blood biomarkers of neurodegenerative diseases

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-08-11 Tau biomarkers

    Blood biomarkers are increasingly used to support the diagnosis and monitoring of neurodegenerative diseases.

    Why it matters

    This cross-sectional study developed population-based reference equations and Z-scores to help interpret blood biomarkers of neurodegenerative diseases, accounting for factors such as age, sex, body-mass index, and renal function. It is about how to read biomarker results and does not test treatment, cure, or prevention.

  7. Antemortem α-Synuclein levels from neuron-derived extracellular vesicles identify Lewy Body pathology in Parkinson’s Disease and Alzheimer Disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-08-05 Tau biomarkers

    These aggregated proteins contribute to the pathological and clinical heterogeneity of AD and are associated with a more rapid progression.

    Why it matters

    This work examined α-synuclein levels from neuron-derived extracellular vesicles as a way to identify Lewy body pathology in Parkinson's disease and Alzheimer's disease, since current biomarkers such as cerebrospinal fluid measurement or skin biopsy are invasive and not easily scalable. It is a biomarker approach and does not treat, cure, or prevent Alzheimer's disease.

  8. The Metabolome as a Readout for Adverse Social Exposome Influences on Human Health - A Roadmap for Modifiable Factors and Proactive Health

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv : the preprint server for health sciences 2026-02-12 Risk factors

    The exposome factors, such as diet, lifestyle, microbiome, chemical exposures and social exposome, shapes human health beyond genetic influences, but the mechanisms remain only partially understood.

    Why it matters

    This study found that people living in adverse social exposome conditions had metabolic features often linked to higher risks for cardiovascular diseases and cognitive decline. It maps possible modifiable factors but does not test any treatment, cure, or prevention for Alzheimer's disease.

  9. RETRACTED: Revolutionizing medical imaging: A cutting-edge AI framework with vision transformers and perceiver IO for multi-disease diagnosis

    ⚠ Retracted — do not rely on it alzhub usefulness score 16 out of 100. Computational Biology and Chemistry 2025-07-04 Brain scans and imaging

    The integration of artificial intelligence in medical image classification has significantly advanced disease detection.

    Why it matters

    This paper is marked as retracted, so its reported framework and claims about early disease detection should not be relied upon. No usable evidence about treating, curing or preventing Alzheimer's disease can be drawn from it.

  10. A head-to-head comparison of multiple amyloid PET radiotracers for Down syndrome clinical trials

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2025-03-19 Down syndrome and Alzheimer's

    Adults with Down syndrome carry high risk of developing Alzheimer’s disease and efforts to include this population in clinical trials remain limited.

    Why it matters

    This head-to-head comparison of amyloid PET radiotracers in 237 adults with Down syndrome found that PiB had the largest effect size for measuring amyloid change while florbetapir had a small effect size. It is a methods comparison for trial screening and tests no treatment or prevention.

  11. Cassava Sciences Topline Phase 3 Data Did Not Meet Co-Primary Endpoints (ReThink-ALZ)

    ⚠ Press release — not a study alzhub usefulness score 16 out of 100. GlobeNewswire (company press release); trial registered as NCT04994483 2024-11-25 Clinical trials

    This was the pivotal, large-scale trial meant to prove whether simufilam, a controversial experimental Alzheimer's drug, actually works.

    Why it matters

    This was the pivotal, large-scale trial meant to prove whether simufilam, a controversial experimental Alzheimer's drug, actually works, and it did not: people taking the drug declined at essentially the same rate as those on placebo on both the cognitive test and the daily-function test. It missed every pre-specified endpoint, cognitive, functional, and biomarker.

  12. Retraction Note: A specific amyloid-beta protein assembly in the brain impairs memory

    ⚠ Retracted — do not rely on it alzhub usefulness score 16 out of 100. Nature 2024-06-24 Laboratory science

    Eighteen years after it was published, Nature formally retracted the landmark 2006 paper that had proposed a specific amyloid protein (Aβ*56) as a cause of memory loss in mice, citing evidence of image manipulation, including splicing, duplication, and use of an image-editing 'eraser' tool.

    Why it matters

    This retraction removes a widely cited claim that a specific amyloid protein assembly called Aβ*56 causes memory loss in mice, because the paper's images were found to be manipulated. It does not by itself disprove the amyloid hypothesis, but it means this particular piece of supporting evidence can no longer be trusted.

  13. A disease similarity approach identifies short-lived Niemann-Pick type C disease mice with accelerated brain aging as a novel mouse model for Alzheimer’s disease and aging research

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2024-04-23 Down syndrome and Alzheimer's

    Since its first description in 1906 by Dr. Alois Alzheimer, Alzheimer’s disease (AD) has been the most common type of dementia.

    Why it matters

    This study proposes short-lived Niemann-Pick type C disease mice with accelerated brain aging as a new mouse model for Alzheimer's disease and aging research. It is animal model work and reports no treatment, cure, or prevention in people.

  14. Reduction in neurons immunoreactive for parvalbumin, calretinin and calbindin in the anteroventral thalamic nuclei of individuals with Down syndrome

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2024-02-02 Down syndrome and Alzheimer's

    The anterior thalamic nuclei are important for cognition, and memory in particular.

    Why it matters

    This post-mortem study found fewer neurons expressing parvalbumin, calretinin and calbindin in the anteroventral thalamic nucleus of people with Down syndrome. It describes a change in brain tissue associated with Down syndrome but does not test any treatment, cure or prevention for Alzheimer's disease.

  15. Modeling Down syndrome neurodevelopment with isogenic cerebral organoids

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2022-05-26 Down syndrome and Alzheimer's

    As a model of early fetal brain development in Down syndrome, this study examines cortical organoids generated from isogenic trisomic and disomic iPSC lines.

    Why it matters

    This study used isogenic cerebral organoids to model early fetal brain development in Down syndrome and found broad differences in gene activity. It is a laboratory model of neurodevelopment and does not test any treatment, cure or prevention for Alzheimer's disease.

  16. Chr21 protein-protein interactions: enrichment in products involved in intellectual disabilities, autism and Late Onset Alzheimer Disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2019-12-12 Down syndrome and Alzheimer's

    Intellectual disability (ID) found in Down syndrome (DS), which is characterized by an extra copy of 234 genes on Chr21 is poorly understood.

    Why it matters

    Using Down syndrome mouse models and a large yeast two-hybrid screen, this study identified many new protein-protein interactions involving chromosome 21 proteins. It is basic molecular research and does not test any treatment, cure or prevention for Alzheimer's disease.

  17. RETRACTED: Hesperetin, a Citrus Flavonoid, Attenuates LPS-Induced Neuroinflammation, Apoptosis and Memory Impairments by Modulating TLR4/NF-κB Signaling

    ⚠ Retracted — do not rely on it alzhub usefulness score 16 out of 100. Nutrients 2019-03-17 Biomarkers

    Glial activation and neuroinflammation play significant roles in apoptosis as well as in the development of cognitive and memory deficits.

    Why it matters

    This paper has been retracted, so its findings on hesperetin in a lipopolysaccharide model cannot be relied on. Even as originally reported, it was a preclinical laboratory and animal study, not evidence that hesperetin treats or prevents Alzheimer's disease in people.

  18. Passive immunization reduces behavioral and neuropathological deficits in an alpha-synuclein transgenic model of Lewy body disease

    ⚠ Retracted — do not rely on it alzhub usefulness score 16 out of 100. PloS one 2011-04-29 Lewy body dementia

    Dementia with Lewy bodies (DLB) and Parkinson's Disease (PD) are common causes of motor and cognitive deficits and are associated with the abnormal accumulation of alpha-synuclein (α-syn).

    Why it matters

    In an alpha-synuclein transgenic model, passive immunization with the antibody 9E4 reduced behavioural deficits and alpha-synuclein accumulation and promoted clearance via the lysosomal pathway. It is animal research, so it does not yet show any treatment, cure or prevention for Alzheimer's disease.

  19. Selective molecular alterations in the autophagy pathway in patients with Lewy body disease and in models of alpha-synucleinopathy

    ⚠ Retracted — do not rely on it alzhub usefulness score 16 out of 100. PloS one 2010-02-19 Lewy body dementia

    This study supports the notion that defects in the autophagy pathway and more specifically in mTor and Atg7 are associated with neurodegeneration in DLB cases and alpha-synuclein transgenic models and supports the possibility that modulators of the autophagy pathway might have potential therapeutic effects.

    Why it matters

    In brains from people with dementia with Lewy bodies, levels of mTor were elevated and Atg7 reduced compared with controls and Alzheimer's disease, and similar changes appeared in alpha-synuclein transgenic mice, where rapamycin or an Atg7 vector reduced alpha-synuclein accumulation. This is tissue and animal work on autophagy, not a treatment tested in patients.

  20. Mutations in mitochondrial cytochrome c oxidase genes segregate with late-onset Alzheimer disease

    ⚠ Retracted — do not rely on it alzhub usefulness score 16 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1997-04-01 Brain tissue and pathology

    Mounting evidence suggests that defects in energy metabolism contribute to the pathogenesis of Alzheimer disease (AD).

    Why it matters

    This study searched mitochondrial genes, including CO1 and CO2, for mutations that might alter cytochrome c oxidase activity and cosegregate with late-onset Alzheimer's disease. It is genetic research into a possible disease mechanism and does not provide a treatment, cure, or prevention.

  21. Kisunla (donanemab) — EU Marketing Authorization (EPAR), following CHMP re-examination

    ⚠ Regulatory decision — not a study alzhub usefulness score 15 out of 100. European Medicines Agency 2025-09-24 Treatments

    The EMA initially recommended against approving donanemab in March 2025, again on ARIA risk-benefit grounds, then reversed itself after re-examination: the CHMP issued a positive opinion on July 24, 2025, and the European Commission granted marketing authorization on September 24, 2025, restricted to early-Alzheimer's patients with one or no copy of the ApoE4 gene.

    Why it matters

    The EMA initially recommended against approving donanemab on ARIA risk-benefit grounds, then reversed itself and granted EU authorization restricted to early-Alzheimer's patients with one or no copy of the ApoE4 gene. The EU label excludes several groups including patients on anticoagulants and caps treatment at 18 months.

  22. Retraction: High-Affinity Naloxone Binding to Filamin A Prevents Mu Opioid Receptor-Gs Coupling / Retraction: Naloxone's Pentapeptide Binding Site on Filamin A Blocks Mu Opioid Receptor-Gs Coupling (among five Wang-authored papers retracted)

    ⚠ Retracted — do not rely on it alzhub usefulness score 12 out of 100. PLOS ONE 2022-03-30 Laboratory science

    Following an anonymous 2021 whistleblower petition to the FDA alleging manipulated research underlying the Alzheimer's drug simufilam, PLOS ONE conducted its own investigation and retracted five papers co-authored by Hoau-Yan Wang, some of them co-authored with a Cassava Sciences executive, after finding that background patterns in blot images appeared 'more similar than would be expected for data obtained in independent experiments.'

    Why it matters

    Five papers by Hoau-Yan Wang, some co-authored by a Cassava Sciences executive, were retracted after blot image backgrounds looked more similar than expected for independent experiments. These retractions removed published laboratory support for the simufilam research program, and Wang disputed them while an institutional investigation covering roughly 20 papers proceeded.

  23. Hydrogen-rich saline improves memory function in a rat model of amyloid-beta-induced Alzheimer's disease by reduction of oxidative stress

    ⚠ Retracted — do not rely on it alzhub usefulness score 11 out of 100. Brain research 2010-02-19 Biomarkers

    This study is to examine if hydrogen-rich saline reduced amyloid beta (Abeta) induced neural inflammation, and learning and memory deficits in a rat model.

From across this topic

10 of the 4,930 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.

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