In Alzheimer's disease, tau pathology spreads across brain regions as the disease progresses. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
In Alzheimer's disease, tau pathology spreads across brain regions as the disease progresses. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Unlike other aggregation inhibitors, RI-AG03 effectively suppresses aggregation of multiple Tau species containing both hotspots in vitro and in vivo, is non-toxic, and suppresses aggregation-dependent neurodegenerative and behavioral phenotypes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Monoclonal antibodies have emerged as a leading therapeutic agent for the treatment of disease, including Alzheimer's disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a major cause of morbidity worldwide and its prevalence is expected to rise. 1 key finding →
Evidence: high
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is the most common form of dementia; however, its molecular mechanisms are not fully understood. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Immunotherapies targeting extracellular tau share the premise that interrupting cell-to-cell spread of tau pathology in Alzheimer's disease (AD) will slow dementia pathogenesis. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurons with lower basal UPS activity were more vulnerable to tau accumulation following mild UPS inhibition. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The relationship between amyloid-β (Aβ) species and tau pathology in Alzheimer's disease (AD) is not fully understood. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Excitatory neurons are preferentially impaired in early Alzheimer's disease but the pathways contributing to their relative vulnerability remain largely unknown. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The accumulation of pathological misfolded tau is a feature common to a collective of neurodegenerative disorders known as tauopathies, of which Alzheimer's disease (AD) is the most common. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tauopathies are neurodegenerative diseases characterized by aberrant forms of tau protein accumulation leading to neuronal death in focal brain areas. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Ligands targeting tau for use with positron emission tomography have rapidly been developed during the past several years, enabling the in vivo study of tau pathology in patients with Alzheimer's disease and related non-Alzheimer's disease tauopathies. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Extracellular deposition of amyloid-β as neuritic plaques and intracellular accumulation of hyperphosphorylated, aggregated tau as neurofibrillary tangles are two of the characteristic hallmarks of Alzheimer's disease 1,2 . 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The term "propagon" is used to define proteins that may transmit misfolding in vitro, in tissues or in organisms. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is characterized by the deposition of amyloid-β as extracellular plaques and hyperphosphorylated tau as intracellular neurofibrillary tangles. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tauopathies are neurodegenerative diseases characterized by the intraneuronal accumulation of aggregated tau. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Traumatic brain injury (TBI) is characterized by acute neurological dysfunction and associated with the development of chronic traumatic encephalopathy (CTE) and Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In Alzheimer's disease (AD) and other tauopathies, the cytosolic protein Tau misfolds and forms intracellular aggregates which accumulate within the brain leading to neurodegeneration. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurofibrillary tangles (NFTs), composed of truncated and hyperphosphorylated tau, are a common feature of numerous aging-related neurodegenerative diseases, including Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
It is unclear whether Alzheimer disease pathology drives cognitive decline in Parkinson disease (PD) patients carrying GBA1 variants. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
To assess the ability of [18F]PI-2620 to detect regional tau burden in non-Alzheimer's disease tauopathies compared with Alzheimer's disease, patients with progressive supranuclear palsy (n = 3), corticobasal syndrome (n = 2), corticobasal degeneration (n = 1) or Alzheimer's disease (n = 8), and healthy controls (n = 7) were recruited. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This study focused on designing and evaluating Tau-PET tracers for noninvasive positron emission computed tomography (PET) imaging of neurofibrillary tangles (NFTs), a hallmark pathology of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This article introduces an alternative immunodiagnostic approach based on the concept of a "tauosome" - the diverse set of tau fragments present within biological fluids. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The aggregation of amyloid-beta peptide and tau protein dysregulation are implicated to play key roles in Alzheimer's disease pathogenesis and are considered the main pathological hallmarks of this devastating disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau is a microtubule associated protein in the brain that aggregates in Alzheimer's disease to form pathological tangles and neurites. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
8 of the 401 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 8. The same 8 appear here every time.
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
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.
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 30,980 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.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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