28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
CSF phospho-tau (p-tau(181)) levels have shown good diagnostic utility in differential diagnosis of Alzheimer disease (AD). 4 key findings →
Evidence: low
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Mutations in the presenilin 1 (PS1) gene (PSEN1) are associated with familial Alzheimer disease (FAD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Cortical posterior hypometabolism on PET imaging with 18 F-FDG (FDG-PET), and altered levels of Aß 1-42 peptide, total Tau (tTau) and phosphorylated Tau (pTau) proteins in cerebrospinal fluid (CSF) are established diagnostic biomarkers in Alzheimer's disease (AD). 4 key findings →
Participants: 120 Evidence: low
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The measurement of CSF specimens from Netherlands Brain Bank showed that the levels of total tau and p-tau in CSF specimens of AD patients were significantly higher than those in CSF of patients with VD and non-dementia neurological disorders, and of age-matched non- 4 key findings →
Participants: 52 Evidence: low
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In recent studies, patients diagnosed with Alzheimer's disease (AD) showed significantly elevated CSF levels of tau protein. 4 key findings →
Participants: 132 Evidence: low
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Older adults with MDD were more likely to endorse MBI. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In the study scenario, adding plasma p -tau217 testing to SCE reduced diagnostic costs by $342/patient, through more efficient use of amyloid PET and CSF testing. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
To evaluate plasma p-tau217 ability to detect pre-symptomatic Alzheimer disease (AD) in ethnoracially diverse cognitively normal individuals. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
In Part 1 (currently ongoing), between February 6, 2024, and December 27, 2024, 322 adults were screened, of whom 75 (aged 59-89 years) met NIA-AA and IPA criteria. 5 key findings →
Design: clinical trial Participants: 322 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The approval of disease-modifying treatments for Alzheimer's disease demands a rethinking of cognitive screening. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We recently identified a cDNA encoding a human brain specific trypsinogen (trypsinogen IV). 2 key findings →
Evidence: low
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Previous studies have shown a marked decline in neuronal and an increase in glial gene expression in Alzheimer's disease (AD) neocortex. 2 key findings →
Evidence: low
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Neuropsychological assessments are essential to define the cognitive profile and contribute to the diagnosis of Alzheimer's disease (AD). 4 key findings →
Evidence: low
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We performed a retrospective analysis of the patients assessed at our memory unit for whom Alzheimer disease (AD) cerebrospinal fluid biomarker results were available. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
BackgroundNeighborhood disadvantage has been associated with reduced cognitive reserve, increased risk for cognitive impairment, and greater Alzheimer's disease (AD) neuropathology, with particularly pronounced effects among Black and Hispanic/Latino older adults. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
BackgroundDespite dementia with Lewy bodies (DLB) being the second most common form of neurodegenerative dementia, more than 80% of DLB cases are initially misdiagnosed. 2 key findings →
Evidence: low
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Familial frontotemporal dementia (FTD) is a genetically heterogeneous disease with various clinical manifestations, making it difficult to diagnose. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In 2004, the first radiotracer that bound amyloid plaques was reported, which enabled visualization of the amount and regional distribution of amyloid plaques in the brains of living individuals via positron emission tomography (PET). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Since the term limbic-predominant age-related TDP-43 encephalopathy (LATE) was coined in 2019, more than 200 articles addressing the subject were published. 1 key finding →
Evidence: low
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As the term limbic-predominant age-related transactive response DNA-binding protein 43 (TDP-43) encephalopathy (LATE) was coined in 2019, more than 200 articles addressing the subject were published. 1 key finding →
Evidence: low
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The recent approval of disease-modifying therapies (DMTs) for early Alzheimer's disease (AD) marks a major shift in clinical practice. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Frontotemporal dementia regards a group of presenile progressive neurodegenerative form of dementias which includes Pick's disease, corticobasal degeneration, frontotemporal dementia with motor neuron disease, frontal lobe degeneration, dementia-parkinsonism-amyotrophy complex, familial non-specific dementia mapping to chromosome 3, non-Alzheimer degenerative dementia lacking distinctive histological features as well as a number other infrequent syndromes with dementia and focal neurological signs. 1 key finding →
Evidence: low
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Inositol monophosphatase (IMPase), a cytoplasmic enzyme that hydrolyses inositol monophosphates to produce inositol is also found in the cerebrospinal fluid (CSF). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The existence of an effective biomarker for early detection of Alzheimer disease would facilitate improved diagnosis and stimulate therapeutic trials. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
In accordance with the current German dementia guidelines, the dementia biomarkers amyloid beta 42, the tau peptides total tau and phosphorylated tau 181 are recommended for cerebrospinal fluid (CSF)-based diagnostics of dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
10 of the 3,322 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.
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 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.
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 →