Tauopathies are neurodegenerative diseases characterized by pathological tau protein inclusions and dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Tauopathies, such as Alzheimer's disease and frontotemporal dementia, are common neurodegenerative diseases characterized by misfolding, hyperphosphorylation, and aggregation of tau. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
43/100
This method differentiated eight tauopathies, including Alzheimer's disease, Pick disease, progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), argyrophilic grain disease (AGD), frontotemporal dementia with parkinsonism associated with chromosome 17 with N279K mutation (FTDP-17 N279K), and globular glial tauopathies types II and III. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
LLMD participants were more likely to be tau PET and Aβ PET positive than HCs. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
43/100
These results provide a link between tau autoimmunity and tauopathy-like abnormalities and indicate potential dangers of using tau for immunotherapy. 2 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
Autopsy studies have shown that about 55% of patients with frontotemporal lobar degeneration (FTLD) and 25% of patients with Alzheimer's disease (AD) harbour TDP-43 immunoreactive pathological changes in their brains. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Corticobasal degeneration (CBD) is an adult-onset progressive neurodegenerative disorder characterized by L-dopa-resistant rigidity, focal cortical deficits, and variable dementia. 1 key finding →
Participants: 12 Evidence: low
Full summary, score breakdown and related studies → Original source
Splice-site and missense mutations have been identified in tau associated with frontotemporal dementia with parkinsonism linked to chromosome 17. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
The human tau protein is implicated in a wide range of neurodegenerative "tauopathy" diseases, consisting of Alzheimer's disease (AD) and frontotemporal lobar degeneration which includes progressive supranuclear palsy, corticobasal degeneration, Pick's disease, and FTLD-tau (frontotemporal dementia with parkinsonism caused by MAPT mutations). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Familial frontotemporal dementia (FTD), characterized by tau-negative, ubiquitin-positive inclusions at autopsy, is linked to a chromosomal region at 17q21 (FTDU-17), encompassing the gene encoding the microtubule associated protein tau, MAPT. 2 key findings →
Participants: 17 Evidence: low
Full summary, score breakdown and related studies → Original source
Both CSF tau and CSF phosphotau were increased in probable AD compared with FTD (p<0.001), SAE (p<0.001), PD (p<0.001), and controls (p<0.001). 4 key findings →
Participants: 41 Evidence: low
Full summary, score breakdown and related studies → Original source
The precursor of the non-Abeta-component of Alzheimer's disease (AD) amyloid (NACP, alpha-synuclein) aggregates into insoluble filaments of Lewy bodies (LBs) in Parkinson's disease (PD) and dementia with LBs (DLB). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The antigenic profile of neurofibrillary tangles (NFT) in Alzheimer's disease (AD), senile dementia of Alzheimer type (SDAT), progressive supranuclear palsy (PSP) and in non-demented aged humans was investigated by light and electron microscopic immunocytochemistry using antisera and monoclonal antibodies to tubulin, microtubule-associated proteins (MAP1, MAP2 and tau), neurofilament proteins and determinants unique to Alzheimer paired helical filaments (PHF). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The tau proteins have been reported only in association with microtubules and with ribosomes in situ, in the normal central nervous system. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In normal adult brain the microtubule associated protein (MAP) tau contains 2-3 phosphates per mol of the protein and at this level of phosphorylation it is a soluble cytosolic protein. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cerebrospinal fluid (CSF) tau is a common biomarker for Alzheimer disease (AD). 4 key findings →
Evidence: moderate
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Mild cognitive impairment is considered to be a transitional stage between normal aging and dementia. 4 key findings →
Participants: 16 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Creatine transporter deficiency (CTD) is a rare X-linked disorder of creatine transport caused by pathogenic variants in SLC6A8 (Xq28). 4 key findings →
Participants: 12 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cognitively impaired patients with negative biomarkers of amyloidosis but with neurochemical evidence of Tau pathophysiology or neurodegeneration or both are classified as "suspected non-Alzheimer pathophysiology" (SNAP), according to the 2018 research framework for a biological definition of Alzheimer's disease (AD). 4 key findings →
Participants: 99 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The spreading of MAPT/Tau pathology is closely associated with the progression of neurodegeneration and cognitive decline in Alzheimer disease and other tauopathies. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Aβ + CN individuals performed worse than Aβ-CN participants in the SCBC while the SOC only distinguished Aβ − CN from MCI participants. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Area under the receiver operating characteristic curves differentiating PSP and controls were improved by PC1 subtraction in the frontal white matter (0.54 to 0.67; P = 0.002) and subcortical (0.69 to 0.87; P < 0.001) regions. 4 key findings →
Participants: 141 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
AcTau174 levels were elevated in all dementia groups compared to controls, with a stepwise increase from controls to MCI-AD (2.2-fold) to AD dementia (3.5-fold, Figure 1). 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
TDP-43 is a ubiquitously expressed, primarily nuclear DNA/RNA-binding protein implicated in neurodegenerative diseases including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
42/100
Dietary high salt intake is increasingly recognized as a risk factor for cognitive decline and dementia, including Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
From across this tag
9 of the 734 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 9. The same 9 appear here every time.
- In Vivo Characterization and Quantification of Neurofibrillary Tau PET Radioligand 18F-MK-6240 in Humans from Alzheimer Disease Dementia to Young Controls
- Calcium-mediated transient phosphorylation of tau and amyloid precursor protein followed by intraneuronal amyloid-beta accumulation
- Association of Longitudinal Changes in Cerebrospinal Fluid Total Tau and Phosphorylated Tau 181 and Brain Atrophy With Disease Progression in Patients With Alzheimer Disease
- Phosphorylated Tau in Alzheimer's Disease and Other Tauopathies
- Total Tau and Phosphorylated Tau Protein Serum Levels in Patients with Schizophrenia Compared with Controls
- Reduction of Nuak1 Decreases Tau and Reverses Phenotypes in a Tauopathy Mouse Model
- Tau Suppression in a Neurodegenerative Mouse Model Improves Memory Function
- Detecting amyloid and tau pathology in Parkinson’s disease, 4R-tauopathies and control subjects with plasma pTau217
- Alzheimer's disease profiled by fluid and imaging markers: tau PET best predicts cognitive decline
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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.
1,034 records (3.7% 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 →