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Find studies

Showing 8,301–8,325 of 8,338 studies · tagged Brain Biology (page 333 of 334) · 30,180 in the whole library · How the 0–100 score works

Download bibliography of the first 500 of these studies, in this order: BibTeX (.bib) · RIS (.ris)

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

PDE2A Modulation Attenuates Aβ-Induced Neuronal Injury and Associated Oxidative, Inflammatory, and Apoptotic Responses

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-01

Across cellular and animal Aβ injury models, BML-288 attenuated oxidative and inflammatory disturbances, modulated apoptosis-related protein expression, and improved cognitive outcomes. 2 key findings →

Evidence: low

Micro- and nanoplastics alter electrophysiological brain patterns and reshape human neurodevelopmental trajectories

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100.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

Environmental microplastics and nanoplastics (MNPs) are emerging contaminants that accumulate in human tissues, including the brain, yet their mechanistic impact on the nervous system remains poorly understood. 3 key findings →

Evidence: low

Cell type-specific histone acetylation landscape in Alzheimer’s disease reveals a putative role of MITF in microglia

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-14

Alzheimer’s disease (AD) is characterised by aberrant amyloid beta and tau aggregation, neuroinflammation, demyelination and neurodegeneration, which have been linked to changes in cell-specific gene expression signatures. 2 key findings →

Evidence: low

Forecasting Alzheimer’s disease progression using non-imaging clinical features and XGBoost

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100.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

Machine learning (ML) methods have shown promise in modeling clinical trajectories associated with neurodegenerative disorders such as Alzheimer’s disease (AD). 3 key findings →

Design: longitudinal study Participants: 15,727 Evidence: moderate

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. 5 key findings →

Evidence: low

A reproducibility-audit framework for generalizable versus dataset- specific molecular transition boundaries in Alzheimer’s disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-01

Validated on synthetic ground truth, the audit separates a generalizable anchor (PTGDS) from a dataset-specific signal and a global-expression artefact, providing a reusable control for trajectory-based molecular staging. 5 key findings →

Evidence: moderate

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

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. 1 key finding →

Evidence: low

Underlying histopathology features of white matter hyperintensities in vascular and neurodegenerative disorders: a systematic review

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

White matter hyperintensities (WMHs) are a hallmark of cerebral small vessel disease, commonly seen in cognitively normal older adults and patients with neurodegenerative disorders, and are thought to reflect varying degrees of tissue damage. 2 key findings →

Participants: 45 Evidence: low

Cerebrospinal fluid YWHAG:NPTX2 ratio predicts clinical severity and future phenoconversion in frontotemporal lobar degeneration

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-08-31

Frontotemporal lobar degeneration (FTLD) is a common cause of early-onset dementias marked by progressive declines in behavior, cognition, and/or movement. 3 key findings →

Evidence: low

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

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. 1 key finding →

Evidence: low

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 (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. 2 key findings →

Evidence: low

Neuroinflammation is an early pathological process in a mouse model of prodromal Parkinsons disease

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

Approximately 90% of Parkinson's disease (PD) patients exhibit olfactory deficits, which often precedes motor symptoms by years, and are a robust predictor for PD and subsequent cognitive decline. 3 key findings →

Evidence: low

The neurodegenerative processes underlying Alzheimer’s disease and related dementias (ADRD) begin years before clinical diagnosis, motivating scalable approaches for earlier identification. 3 key findings →

Design: longitudinal study Evidence: moderate

Selective vulnerability of human basal forebrain subsystems in ageing and neuropsychiatric disorders

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-15

These findings identify an anatomically specific age-related profile of the human BF, with structural vulnerability manifest and pre-diagnostic neurological disorders, which is not substantially explained by common inherited risk. 2 key findings →

Design: cross-sectional Evidence: moderate

From across this tag

9 of the 8,313 studies in this tag that have a study page, 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.

↑ Change the filters

Where “Free full text” comes from

Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read

How the 0–100 score works — and why some entries are capped

This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.

  • Journal tier up to 10 pts
  • Journal's citation record up to 4 pts
  • Study design up to 12 pts
  • Strength of evidence up to 5 pts
  • Peer-review validation up to 10 pts
  • How recent up to 5 pts
  • Sample size up to 4 pts
  • Effect reported up to 3 pts
  • Studied in people up to 3 pts
  • Randomised / blinded up to 2 pts
  • Times cited up to 7 pts
  • Citations per year up to 5 pts
  • Impact for its field and year up to 6 pts
  • Cited by studies here up to 6 pts
  • Still being cited up to 4 pts
  • Senior author's track record up to 4 pts
  • Institution's track record up to 3 pts
  • Multi-centre collaboration up to 3 pts
  • Indexed in PubMed up to 2 pts
  • Free to read up to 2 pts

Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.

Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.

We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.

The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.

See the whole rubric drawn out → — four charts covering all 30,180 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.

What this library is — and isn't

This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.

1,037 records (3.4% of the library) are not peer-reviewed — 964 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.

See the full, machine-readable breakdown of this library's coverage →

Newest studies, as a dated timeline →    Atom feed