Hyperphosphorylated tau protein deposits and, inflammatory processes are characteristic components of Alzheimer disease (AD) pathology. 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.
44/100
The percentage of unmetabolized 18 F-T807 in plasma followed a single exponential with a half-life of 17.0 ± 4.2 min. Metabolite-corrected plasma radioactivity concentration fit a biexponential (half-lives, 18.1 ± 5.8 and 2.4 ± 0.5 min). 18 F-T807 in gray matter peaked quickly (SUV > 2 at ∼5 min). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
44/100
The plasma reference graphical analysis appeared to be the optimal method of quantification for 18 F-RO-948, yielding strictly time-consistent values of distribution volume and distribution volume ratio at 90 min against the analyses at 120 and 200 min. The reference tissue graphical analysis and SUV ratio were cross-validated against plasma reference graphical analysis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Tau filaments with distinct morphologies and/or isoform compositions underlie a large number of human neurodegenerative diseases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Tau polymerization into the filaments that compose neurofibrillary tangles is seminal to the development of many neurodegenerative diseases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Loss of synapses and dying back of axons are considered early events in brain degeneration during Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Lack of tau expression has been reported to protect against excitotoxicity and to prevent memory deficits in mice expressing mutant amyloid precursor protein (APP) identified in familial Alzheimer disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neurofibrillary tangles, one of the hallmarks of Alzheimer disease (AD), are composed of paired helical filaments of abnormally hyperphosphorylated tau. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
44/100
Cerebrospinal fluid (CSF) concentrations of amyloid beta(42) (Abeta(42)) peptides and tau proteins may serve as biomarkers for Alzheimer disease (AD). 4 key findings →
Participants: 69 Evidence: low
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However, it remains unknown whether white matter (WM) decline due to AD is associated with specific Tau phosphorylation site(s). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The underlying mechanisms of mild behavioral impairment (MBI), a marker for cognitive impairment and dementia, have remained unclear especially in a multiethnic Asian population. 4 key findings →
Participants: 305 Evidence: low
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Many trials of drugs aimed at preventing or clearing β-amyloid pathology have failed to demonstrate efficacy in recent years and further trials continue with drugs aimed at the same targets and mechanisms. 4 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer’s disease (AD) is a heterogeneous neurodegenerative disorder in which tau neurofibrillary tangles are a pathological hallmark closely associated with cognitive dysfunction and neurodegeneration. 5 key findings →
Participants: 615 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Early isolated functional disruptions in salience/visual networks were present in asymptomatic carriers, along with anterior cingulate gray matter reductions. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Tauopathies encompass a large majority of dementia diagnoses and are characterized by toxic neuronal or glial inclusions of the microtubule-associated protein tau. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
WMH burden positively correlated to Neurofilament-Light (NfL) and pTau181. 5 key findings →
Design: cross-sectional Participants: 583 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
ObjectivePlasma p-Tau217 leaves 30-50% of patients in an indeterminate "gray zone" often requiring A{beta}-PET. 1 key finding →
Participants: 630 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Flortaucipir uptake distinguished individuals with PCA and amnestic AD dementia early in the symptomatic course. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Through analytical validation, this assay demonstrated robust performance across multiple lots, operators, and instruments and could be used as a tool for diagnosing AD. 5 key findings →
Participants: 1,091 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Saturation and competition binding studies of (3)H-THK5117 in post-mortem AD brain tissue showed the presence of multiple binding sites. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Object Damage to axons contributes to postinjury disabilities and is commonly observed following traumatic brain injury (TBI). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Patients with essential tremor (ET) frequently develop concurrent dementia, which is often assumed to represent co-morbid Alzheimer disease (AD). 4 key findings →
Participants: 13 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Nowadays, there is an unmet need for reliable and minimally-invasive diagnosis tools capable of detecting Alzheimer's disease at early stages. 3 key findings →
Participants: 113 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Higher plasma p-tau217, lower Aβ42/40, and their interaction were associated with greater Aβ-PET uptake. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The concomitant depletion of dopaminergic and serotonergic inputs within the hippocampus of C57BL/6N mice provokes a pronounced activation of microglia via the NLRP3-inflammasome pathway, accompanied by increased IL-1β expression. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
From across this tag
10 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 10. The same 10 appear here every time.
- Elevation in Plasma p-tau217 Concentrations Among Blood Donors: An Exploratory Cross-Sectional Study
- Vascular Risk and β-Amyloid Are Synergistically Associated with Cortical Tau
- Activated microglia mitigate Aβ-associated tau seeding and spreading
- Looking into Abnormal Co-Expressions of Tau and TDP-43 in the Realm of Mixed Dementia Types: A Double-Punch Scenario
- Caspase-cleavage of tau is an early event in Alzheimer disease tangle pathology
- Familial multiple system tauopathy with presenile dementia: a disease with abundant neuronal and glial tau filaments
- Evaluation of Copathology and Clinical Trajectories in Individuals With Tau-Clinical Mismatch
- The Validation of Multifactor Model of Plasma Aβ 42 and Total-Tau in Combination With MoCA for Diagnosing Probable Alzheimer Disease
- Trans-cellular propagation of Tau aggregation by fibrillar species
- Genomic architecture of human 17q21 linked to frontotemporal dementia uncovers a highly homologous family of low-copy repeats in the tau region
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 →