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Research

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

Find studies

Showing 226–250 of 424 studies (page 10 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.

Antibody semorinemab reduces tau pathology in a transgenic mouse model and engages tau in patients with Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Science translational medicine 2021-05-01

Tau has become an attractive alternative target for passive immunotherapy efforts for Alzheimer's disease (AD). 1 key finding →

Design: clinical trial Evidence: low

Full summary, score breakdown and related studies → Original source

Identification of structural determinants on tau protein essential for its pathological function: novel therapeutic target for tau immunotherapy in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Alzheimer's research & therapy 2014-08-01

We have discovered defined determinants on mis-disordered truncated tau protein which are responsible for tau oligomerisation leading to neurofibrillary degeneration. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Pathological proteins Tau 64 and 69 are specifically expressed in the somatodendritic domain of the degenerating cortical neurons during Alzheimer's disease. Demonstration with a panel of antibodies against Tau proteins

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Acta neuropathologica 1990-01-01

Bundles of paired helical filaments (PHF) accumulate in the pyramidal neurons that degenerate during Alzheimer's disease. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

Astrocytes expressing hyperphosphorylated tau protein without glial fibrillary tangles in argyrophilic grain disease

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Acta neuropathologica 1999-09-01

Argyrophilic grain disease (AgD), a frequent type of late onset dementia, is characterized by the occurrence of Gallyas-stained neuropil grains in the hippocampus, entorhinal cortex, amygdala and hypothalamus. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Mechanistic Studies of Antibody-Mediated Clearance of Tau Aggregates Using an ex vivo Brain Slice Model

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Frontiers in psychiatry 2011-10-21

Recent studies have shown that immunotherapy clears amyloid beta (Aβ) plaques and reduces Aβ levels in mouse models of Alzheimer's disease (AD), as well as in AD patients. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

The excitotoxin quinolinic acid induces tau phosphorylation in human neurons

✓ Peer-reviewed alzhub usefulness score 40 out of 100. PloS one 2009-07-22

Some of the tryptophan catabolites produced through the kynurenine pathway (KP), and more particularly the excitotoxin quinolinic acid (QA), are likely to play a role in the pathogenesis of Alzheimer's disease (AD). 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

GSK-3beta inhibition reverses axonal transport defects and behavioural phenotypes in Drosophila

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Molecular psychiatry 2004-05-01

The tauopathies are a group of disorders characterised by aggregation of the microtubule-associated protein tau and include Alzheimer's disease (AD) and the fronto-temporal dementias (FTD). 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Inhibition of GSK-3 ameliorates Abeta pathology in an adult-onset Drosophila model of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 40 out of 100. PLoS genetics 2010-09-02

Abeta peptide accumulation is thought to be the primary event in the pathogenesis of Alzheimer's disease (AD), with downstream neurotoxic effects including the hyperphosphorylation of tau protein. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Tau oligomers impair memory and induce synaptic and mitochondrial dysfunction in wild-type mice

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Molecular neurodegeneration 2011-06-06

This study identifies tau oligomers as an acutely toxic tau species in vivo, and suggests that tau oligomers induce neurodegeneration by affecting mitochondrial and synaptic function, both of which are early hallmarks in AD and other tauopathies. 4 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Overexpression of tau protein inhibits kinesin-dependent trafficking of vesicles, mitochondria, and endoplasmic reticulum: implications for Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 40 out of 100. The Journal of cell biology 1998-11-01

The neuronal microtubule-associated protein tau plays an important role in establishing cell polarity by stabilizing axonal microtubules that serve as tracks for motor-protein-driven transport processes. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

A High-Throughput Drug Screening Assay for Anti-Tau Aggregation Using Split GFP and Flow Cytometry

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Scientific reports 2025-06-18

Tau protein aggregation is a hallmark of neurodegenerative diseases, including Alzheimer's disease, making the development of anti-aggregation therapeutics a critical area of research. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Structural Insights and Biological Effects of Glycogen Synthase Kinase 3-specific Inhibitor AR-A014418

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Journal of Biological Chemistry 2003-11-01

Glycogen synthase kinase 3 (GSK3) is a serine/threonine kinase that has been implicated in pathological conditions such as diabetes and Alzheimer's disease. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

An In Vitro Model for Neuroscience: Differentiation of SH-SY5Y Cells into Cells with Morphological and Biochemical Characteristics of Mature Neurons

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Journal of Alzheimer s Disease 2010-06-13

Neuroscience, including research on Alzheimer's disease, is hampered by the lack of suitable in vitro models to study the human nervous system. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

Alzheimer's Disease-Like Tau Neuropathology Leads to Memory Deficits and Loss of Functional Synapses in a Novel Mutated Tau Transgenic Mouse without Any Motor Deficits

✓ Peer-reviewed alzhub usefulness score 40 out of 100. American Journal Of Pathology 2006-08-01

Tau transgenic mice are valuable models to investigate the role of tau protein in Alzheimer's disease and other tauopathies. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

The role of graphene patterning in field-effect transistor sensors to detect the tau protein for Alzheimer's disease: Simplifying the immobilization process and improving the performance of graphene-based immunosensors

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Biosensors & bioelectronics 2021-07-24

We report the improvement in the sensing performance of electrolyte-gated graphene field-effect transistor (FET) sensors capable of detecting tau protein through a simplified, linker-free, anti-tau antibody immobilization process. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source

[18F]-AV-1451 binding profile in chronic traumatic encephalopathy: a postmortem case series

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Acta neuropathologica communications 2019-10-28

Despite the presence of abundant tau aggregates in multiple regions in all CTE brains, only faint or no [18F]-AV-1451 binding signal could be detected by autoradiography. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source

From across this tag

7 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 7. The same 7 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