Accumulation of phosphorylated tau is a key pathological feature of Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Abnormal aggregation of tau in the brain is a major contributing factor in various neurodegenerative diseases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Diverse neurodegenerative disorders are characterized by deposition of tau fibrils composed of conformers (i.e. strains) unique to each illness. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
[ 18 F]PI-2620 was selected for clinical validation. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau PET tracers have enabled in vivo quantification of PHF-tau burden in human brains. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The microtubule-associated protein tau has risk alleles for both Alzheimer's disease and Parkinson's disease and mutations that cause brain degenerative diseases termed tauopathies. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In Alzheimer's disease, neurofibrillary tangle pathology appears to spread along neuronal connections, proposed to be mediated by the release and uptake of abnormal, disease-specific forms of microtubule-binding protein tau MAPT. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings suggest the potential of passive immunization targeting proximal N-terminal domain tau 6-18 as a disease-modifying approach to AD and related tauopathies. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau deposition in the brain is a pathological hallmark of many neurodegenerative disorders, including Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The Alzheimer's disease (AD) therapeutic research is yielding a large number of potent molecules. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although tau has been implicated in diverse neurological diseases, its most pathogenic forms remain to be defined. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau acetylation has recently emerged as a dominant post-translational modification (PTM) in Alzheimer's disease (AD) and related tauopathies. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Misfolded and hyperphosphorylated tau accumulates in several neurodegenerative disorders including Alzheimer's disease, frontotemporal dementia with Parkinsonism, corticobasal degeneration, progressive supranuclear palsy, Down syndrome, and Pick's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings indicate that AD p-Tau-injected 3 × Tg-AD mice represent a practical model to study the seeding and spread of Tau pathology, their effect on Aβ pathology, and the effect of Tau immunotherapy on both Tau and Aβ pathologies. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases such as Alzheimer's disease are characterized by the progressive spreading and accumulation of hyper-phosphorylated tau protein in the brain. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The microtubule-associated protein tau is an attractive therapeutic target for the treatment of Alzheimer's disease and related tauopathies as its aggregation strongly correlates with disease progression and is considered a key mediator of neuronal toxicity. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In addition to a prominent role in glycemic control, glucagon-like peptide 1 (GLP-1) receptor agonists exhibit neuroprotective properties. 3 key findings →
Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source
The paired helical filament (PHF) is the major component of the neurofibrillary deposits that form a defining neuropathological characteristic of Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Progressive supranuclear palsy (PSP), previously believed to be a common cause of atypical parkinsonism, is now recognised as a range of motor and behavioural syndromes that are associated with a characteristic 4-repeat tau neuropathology. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Post-translational modifications (PTMs) on tau have long been recognized as affecting protein function and contributing to neurodegeneration. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
By employing the hybridoma technique, 49 mAbs recognizing Tau (1-22), nine mAbs targeting p-Tau231, one mAb targeting p-Tau217, and two mAbs targeting p-Tau181 were developed. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
To simply and rapidly detect the highly phosphorylated tau protein at threonine 217 (p-tau217) as a precautionary measure against Alzheimer's disease and distinguish it from other neurodegenerative diseases, a novel immunosensor was prepared using luminol as the electrochemiluminescent (ECL) sensing probe reinforced by Au-Cu nanoparticles (Au-Cu NPs). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We found that LFS enhanced p-Tau181 and p-Tau217 in an age-dependent manner in the hippocampus of live rats. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Early clinical symptoms of sporadic Creutzfeldt-Jakob disease (CJD) may overlap with other neurodegenerative diseases like Alzheimer's disease (AD) and frontotemporal degeneration (FTD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
A key hallmark of Alzheimer's disease (AD) is the accumulation of hyperphosphorylated tau in neurofibrillary tangles. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 387 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 10. The same 10 appear here every time.
- Cellular and pathological heterogeneity of primary tauopathies
- Identification of retinal oligomeric, citrullinated, and other tau isoforms in early and advanced AD and relations to disease status
- Pick's disease: hyperphosphorylated tau protein segregates to the somatoaxonal compartment
- From the prion-like propagation hypothesis to therapeutic strategies of anti-tau immunotherapy
- Distinct Therapeutic Mechanisms of Tau Antibodies: Promoting Microglial Clearance Versus Blocking Neuronal Uptake
- TDP-43: From Alzheimer's Disease to Limbic-Predominant Age-Related TDP-43 Encephalopathy
- Aβ deposition is associated with increases in soluble and phosphorylated tau that precede a positive Tau PET in Alzheimer's disease
- Ubiquitin-Proteasome System in the Different Stages of Dominantly Inherited Alzheimer's Disease
- Cell-death pathways and tau-associated neuronal vulnerability in Alzheimer's disease
- Precortical Phase of Alzheimer's Disease (AD)-Related Tau Cytoskeletal Pathology
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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% of the library) are not peer-reviewed — 962 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 →