The microtubule-associated protein Tau plays a critical role in the pathogenesis of Alzheimer disease and several related disorders (tauopathies). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
36/100
Frontotemporal dementia with parkinsonism chromosome 17 type (FTDP-17) is caused by mutations in MAPT, the gene encoding tau. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurofibrillary lesions made of hyperphosphorylated microtubule-associated protein tau constitute not only one of the defining neuropathological features of Alzheimer disease but also are present in a number of other neurodegenerative diseases with dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We generated several cell models of tauopathy in order to study the mechanisms of neurodegeneration in diseases involving abnormal changes of tau protein. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau toxicity has been implicated in the emergence of synaptic dysfunction in Alzheimer's disease (AD), but the mechanism by which tau alters synapse physiology and leads to cognitive decline is unclear. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We describe two new transgenic mouse lines for studying pathological changes of Tau protein related to Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
36/100
Our aging society is confronted with a dramatic increase of patients suffering from tauopathies, which include Alzheimer disease and certain frontotemporal dementias. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Argyrophilic grain disease (AGD) was first reported as an adult-onset dementia, but recent studies have emphasized personality change, emotional imbalance, and memory problems as clinical features of AGD. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In Alzheimer's disease and related disorders, the microtubule-associated protein Tau is abnormally hyperphosphorylated and aggregated into neurofibrillary tangles. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The R406W tau mutation found in frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17) causes a hereditary tauopathy clinically resembling Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microtubule-associated protein tau is the major component of the neurofibrillary tangles of Alzheimer disease (AD) and is genetically linked to frontotemporal dementias (FTDP-17). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Parkinson's disease (PD), a progressive neurodegenerative disease, results in abnormal accumulation of insoluble alpha-synuclein (alpha-Syn) in dopaminergic neurons. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Pathological tau leads to dementia and neurodegeneration in tauopathies, including Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Increased Tau protein amyloidogenicity has been causatively implicated in several neurodegenerative diseases, collectively called tauopathies. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tauopathies are a class of neurodegenerative disorders characterized by neuronal and/or glial inclusions composed of the microtubule-binding protein, tau. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Filamentous tau inclusions in neurons and glia are neuropathological hallmarks of sporadic and familial tauopathies. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
36/100
Intracellular accumulations of filamentous tau inclusions are neuropathological hallmarks of neurodegenerative diseases known as tauopathies. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The synaptic connections that form between neurons during development remain plastic and able to adapt throughout the lifespan, enabling learning and memory. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The microtubule binding protein tau is implicated in neurodegenerative tauopathies, including frontotemporal dementia (FTD) with Parkinsonism caused by diverse mutations in the tau gene. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurofibrillary tangles (NFTs) are a pathological hallmark of many neurodegenerative diseases including Alzheimer's disease (AD), Parkinson's disease (PD), and frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP17). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Sanfilippo syndrome type B (mucopolysaccharidosis III B, MPS III B) is an autosomal recessive, neurodegenerative disease of children, characterized by profound mental retardation and dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Traumatic brain injury (TBI) is a serious problem that affects millions of people in the United States alone. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
36/100
Argyrophilic grain disease (AgD) is a late-onset dementia morphologically characterized by the presence of abundant spindle-shaped argyrophilic grains (ArG) in neuronal processes and coiled bodies in oligodendrocytes. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We report a Japanese family with early onset hereditary frontotemporal dementia and a novel missense mutation (Ser305Asn) in the tau gene. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau protein in a hyperphosphorylated state makes up the intracellular inclusions of several neurodegenerative diseases, including Alzheimer's disease and cases of frontotemporal dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 750 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.
- Distinct tau PET patterns in atrophy-defined subtypes of Alzheimer's disease
- Progressive supranuclear palsy pathology caused by a novel silent mutation in exon 10 of the tau gene: expansion of the disease phenotype caused by tau gene mutations
- Integrating MRI Volume and Plasma p-Tau217 for Amyloid Risk Stratification in Early-Stage Alzheimer Disease
- Diagnostic value of plasma phosphorylated tau181 in Alzheimer's disease and frontotemporal lobar degeneration
- Abnormal tau induces cognitive impairment through two different mechanisms: synaptic dysfunction and neuronal loss
- Topographic Distribution of Amyloid-β, Tau, and Atrophy in Patients With Behavioral/Dysexecutive Alzheimer Disease
- Glycated tau protein in Alzheimer disease: a mechanism for induction of oxidant stress
- Preanalytical stability of plasma/serum brain-derived tau
- Plasma Phosphorylated Tau at Threonine 181 and Neuropsychiatric Symptoms in Preclinical and Prodromal Alzheimer Disease
- Tau-PET is superior to phospho-tau when predicting cognitive decline in symptomatic AD patients
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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →