31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Molecular chaperones, ubiquitin ligases and proteasome impairment have been implicated in several neurodegenerative diseases, including Alzheimer's and Parkinson's disease, which are characterized by accumulation of abnormal protein aggregates (e.g. tau and alpha-synuclein respectively). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microtubule-associated protein tau undergoes several post-translational modifications and aggregates into paired helical filaments (PHFs) in Alzheimer's disease (AD) and other tauopathies. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is a progressive degenerative dementia characterized by the abundant presence of neurofibrillary tangles in neurons. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau is an axonal microtubule-associated protein involved in microtubule assembly and stabilization. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
While the presence of naturally occurring antibodies (Abs) against amyloid-beta in AD patients and healthy subjects have been repeatedly reported, no data on the presence of naturally occurring Abs against tau protein, in its unphosphorylated as well as its pathologically phosphorylated state, has been reported so far. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In this study, we present the detection of tau protein, at room temperature, using a multi-spot localised surface plasmon resonance (LSPR)-based immunochip. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The role of humoral immunity related to neuron- and disease-specific cytoskeletal proteins patients with Alzheimer disease (AD) is unknown. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The neuronal protein tau, a member of the class of intrinsically disordered proteins, is characterized by the absence of any firm 3-D structure and high solubility when free in solution. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Six hours after heat shocking 2- to 3-month-old male and female Sprague-Dawley rats at 42 degrees C for 15 min, we analyzed tau protein immunoreactivity in SDS extracts of cerebrums and peripheral nerves by using immunoblot analysis and immunohistochemistry with the anti-tau monoclonal antibody Tau-1, which recognizes a phosphate-dependent non-phosphorylated epitope, and with 125I-labeled protein A. In the cerebral extracts, we found altered phosphorylation of tau in heat-shocked females, characterized by a marked reduction in the amount of nonphosphorylated tau, a doubling of the ratio of total (phosphorylated plus nonphosphorylated) tau to nonphosphorylated tau, and the appearance of the slowest moving phosphorylated tau polypeptide (68 kDa). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In addition to neuritic changes and amyloid deposits, neuronal and glial cell apoptosis is an important pathological feature of Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Abnormal tau proteins (PHF-tau) were isolated from Alzheimer's disease brains by treatment of paired helical filament enriched-fractions with perchloric acid and boiling of the acid precipitable fraction with beta-mercaptoethanol. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is a significant burden to society. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Two proteins immunologically related to porcine tau protein are found in the brain of Alzheimer's disease patients. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microtubule-associated tau proteins are hyperphosphorylated in brains from patients with Alzheimer's disease compared with normal adult human brain. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The latest therapeutic approaches to Alzheimer disease are using intravenous immunoglobulin (IVIG) products. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurofibrillary tangles (NFT) in Alzheimer's disease (AD) are composed of abnormally phosphorylated tau proteins. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The syndrome of frontotemporal dementia represents a diverse group of diseases presenting with behavioral and cognitive disturbances. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We identified significant clusters of tau-aggregation in praxis-related regions (e.g., supramarginal gyrus, angular gyrus, temporal, parietal and occipital regions) that were associated with apraxia. 4 key findings →
Participants: 32 Evidence: low
Full summary, score breakdown and related studies → Original source
Heterogeneous nuclear ribonucleoprotein A2/B1 (hnRNPA2/B1) is an RNA-binding protein that mislocalizes to the cytoplasm and forms stress-induced granules in tauopathy and multisystem proteinopathy. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microtubule-associated protein tau is an intrinsically disordered protein (IDP) that forms characteristic fibrillar aggregates in several diseases, the most well-known of which is Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau pathology, characterized by the aberrant aggregation and accumulation of tau in neurons and glial cells, plays a critical role in the onset and progression of multiple neurodegenerative diseases. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This study explored the role of the ubiquitin-proteasome system (UPS) in dominantly inherited Alzheimer's disease (DIAD) by examining changes in cerebrospinal fluid (CSF) levels of UPS proteins along with disease progression, AD imaging biomarkers (PiB PET, tau PET), neurodegeneration imaging measures (MRI, FDG PET), and Clinical Dementia Rating® (CDR®). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
NOS1AP is a genetically validated driver of tau pathology in Alzheimer’s disease (AD), yet the NOS1AP-tau interaction itself has remained pharmacologically untargeted. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
SHED exosome treatment demonstrated genotype-specific efficacy, selectively reducing p181-tau levels and restoring the p181-tau/Aβ42 ratio in FAD lines while elevating the protective Aβ42/Aβ40 ratio across both FAD and SAD backgrounds. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The rs28834970 regulatory variant was identified as the most functionally relevant in our model, with the C risk allele promoting transcription factor C/EBPβ binding within a cis-regulatory element. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
9 of the 424 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 9. The same 9 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 31,380 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.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.
1,048 records (3.3% of the library) are not peer-reviewed — 973 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