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Research

31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 401–424 of 424 studies (page 17 of 17) · 31,380 in the whole library · How the 0–100 score works

Download bibliography of these 424 studies, in this order: BibTeX (.bib) · RIS (.ris)

Showing 424 studies tagged tau-protein — clear

Browse by subject, author or institution

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

Subjects

Authors

Names as each record prints them; the same person can appear under two spellings.

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.

Cofilin Suppresses Tau-Induced Defects in Dense-Core Granule Formation and Aβ-Induced Neurodegeneration

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-27

Intracellular neurofibrillary tangles formed from hyperphosphorylated tau and extracellular amyloid plaques containing aggregated Aβ-peptides, specific cleavage products of the Amyloid Precursor Protein (APP), are the primary histopathological hallmarks of Alzheimer’s Disease (AD), the leading cause of dementia in humans. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

APH-1A and CDK5 Expression Correlates with Tau Hyperphosphorylation and Its Attenuation by Brahmi and Donep-M in STZ induced Alzheimer’s Disease Model

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-31

Alzheimer’s disease (AD) is a progressively characterized neurodegenerative condition marked by molecular instability, neuronal dysfunction and abnormal tau buildup. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Opposing Regulation of Tau Condensation by Phosphorylation Levels and Molecular Chaperone Interactions

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100.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

Aggregation of the microtubule-stabilizing protein Tau into insoluble deposits is characteristic for several neurodegenerative diseases, including Alzheimer's disease. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Active amyloid beta immunization ameliorates synapse loss and phosphorylated-tau accumulation around remaining plaques for up to 14 years after treatment

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100.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

Amyloid plaques, one of the defining features of Alzheimer’s disease, are associated with synapse loss and accumulation of pathological tau in dystrophic neurites and reactive glia in their immediate vicinity. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Evaluation of [18F]MK-6240 binding to tau protein in postmortem human brains of Down syndrome and Alzheimer’s disease and assessment of off-target (non-tau) binding

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

Alzheimer's disease (AD) and Down Syndrome (DS) are characterized by the aggregation of tau tangles. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Conformation-based detection of tau seeds with a novel VHH

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2025-12-08

In Alzheimer’s disease (AD) and related tauopathies, progressive pathology has been linked to prion mechanisms whereby ordered tau assemblies, or “seeds,” form in one cell and transit to neighboring or connected cells where they serve as templates for their own replication. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

mRNA vaccine platform demonstrates potent immunotherapeutic targeting of amyloid-β and tau pathologies in Alzheimer's disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2025-09-16

Current Alzheimer’s disease (AD) immunotherapeutics face efficacy and safety limitations with antibody-based approaches. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

In silico design and physicochemical characterisation of a dual-action intranasal nanoparticle formulation for Alzheimer’s disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-09-28

Approved Alzheimer’s disease therapies fail to address the two drivers of cognitive decline: loss of BDNF-TrkB signalling and accumulation of hyperphosphorylated tau protein. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Chronic orexin receptor antagonism is associated with rescued sleep and agitation-like behaviour in tau transgenic PS19 mice, but sex-dependently improved cognition

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Authorea Preprints 2026-07-25

DORA-22 and MK-1064 rescued tauopathy-related sleep loss, and reduced agitation-like locomotion and stress-induced hyperthermic responses. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Depth-Dependent Alterations in Cerebral Blood and Tissue Oxygenation Associated with Tau in Alzheimer’s Disease Models

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

Vascular dysfunction is increasingly recognized as a feature of Alzheimer’s disease (AD), and inadequate oxygen delivery may contribute to neuronal death. 5 key findings →

Design: longitudinal study Evidence: moderate

Full summary, score breakdown and related studies → Original source

Neuronal Hyperactivity Induces Tau Phosphorylation Selectively in Excitatory Pyramidal Neurons Which Contributes to GluA2 Regulation

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

While tau plays a role in regulating neuronal network excitability, a process thought to be dysregulated in Alzheimer’s disease (AD), the molecular mechanisms linking tau and hyperexcitability remain unclear. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Soluble pathogenic tau transmission to astrocytes drives cellular senescence and neurovascular uncoupling in a model of Alzheimer’s tauopathy

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-09-12

Pathogenic tau oligomers are transmitted between neurons and non-neuronal cells and may contribute to cellular dysfunction in Alzheimer’s disease (AD). 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Disease-specific tangle immunophenotypes distinguish hippocampal vulnerability in Alzheimer’s disease and Parkinson’s disease dementia

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-08-19

Structured Abstract INTRODUCTION Tau pathology typically occurs in Alzheimeŕs disease (AD), however is also frequently present in Parkinsońs disease dementia (PDD) and Dementia with Lewy Bodies (DLB), yet its disease-specific signature is unclear. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Neuron tau-targeting biomimetic nanoparticles for curcumin delivery to delay progression of Alzheimer's disease

⚠ Retracted — do not rely on it alzhub usefulness score 15 out of 100. Journal of nanobiotechnology 2020-05-13

Intravenous neuronal tau-targeted T807-modified novel biomimetic nanosystems are a promising clinical candidate for the treatment of AD. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

From across this tag

10 of the 424 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 10. The same 10 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 31,380 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 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.

1,048 records (3.3% of the library) are not peer-reviewed — 973 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    Where this research is being discussed: events