32,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Neurofilament light (NfL) is a marker of neuroaxonal injury, a prominent feature of Alzheimer's disease. 4 key findings →
Design: cross-sectional Participants: 1,149 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Studies evaluating the diagnostic test accuracy of plasma phosphorylated tau (p-tau) and amyloid beta (Aβ) tests (p-tau217, %p-tau217, p-tau181, p-tau231, and Aβ42/Aβ40) compared to reference standard tests (cerebrospinal fluid [CSF] AD biomarkers, amyloid positron emission tomography [PET], or neuropathology) in individuals with cognitive impairment (mild cognitive impairment or dementia) in specialized care settings were included. 4 key findings →
Design: meta-analysis Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Pericyte damage, reflected by CSF PDGFRβ, may be involved in age-related BBB disruption together with neuroinflammation, but is not related to Alzheimer-related pathologic changes. 2 key findings →
Participants: 408 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Using the Swedish BioFINDER-2 cohort [n = 1702, 50.7% male, mean (standard deviation) age 68.4 (12.2) years], we compared the associations between tau/Aβ-PET load and fluid biomarkers alone versus biomarkers in a ratio with a reference protein (Aβ40 or np-tau) in univariate linear regression models. 5 key findings →
Design: longitudinal study Participants: 1,702 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Anti-amyloid treatments for early symptomatic Alzheimer disease have recently become clinically available in some countries, which has greatly increased the need for biomarker confirmation of amyloid pathology. 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A tau/Aβ42 ratio of >0.52 constitutes a robust cerebrospinal fluid Alzheimer profile. 3 key findings →
Participants: 1,442 Evidence: moderate
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CSF biomarkers, including P-tau, T-tau, Aβ 42 , Aβ 40 , and NFL, support in vivo identification of AD neuropathology and correlate with FTLD neuropathology. 4 key findings →
Participants: 101 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Core CSF changes in Alzheimer disease (AD) are decreased amyloid β(1-42), increased total tau, and increased phospho-tau, probably indicating amyloid plaque accumulation, axonal degeneration, and tangle pathology, respectively. 4 key findings →
Design: cross-sectional Participants: 529 Evidence: moderate
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The CSF Aβ42/Aβ40 and Aβ42/Aβ38 ratios are significantly better than CSF Aβ42 to detect brain amyloid deposition in prodromal AD and to differentiate AD dementia from non-AD dementias. 5 key findings →
Participants: 1,182 Evidence: low
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The aim of this study was to evaluate longitudinal associations of multimodal core 1 AD biomarkers with cognition in a cognitively unimpaired (CU) population at increased risk of AD dementia. 4 key findings →
Design: longitudinal study Participants: 350 Evidence: moderate
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This review presents an overview of the latest advances in the field of biomarkers for neurodegenerative diseases. 3 key findings →
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Ascertainment of the -synuclein level in CSF somewhat improves the differential diagnosis of AD vs DLB and PDD when combined with established AD biomarkers. 3 key findings →
Design: cross-sectional Participants: 453 Evidence: low
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During follow-up, 57 (42%) patients with MCI developed Alzheimer's disease, 21 (15%) developed other forms of dementia, and 56 (41%) remained cognitively stable for 5.2 years (range 4.0-6.8). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Widespread implementation of cerebrospinal fluid (CSF) biomarkers of Alzheimer's disease (AD) in clinical settings requires improved accuracy for diagnosis of prodromal disease and for distinguishing AD from non-AD dementias. 4 key findings →
Participants: 338 Evidence: moderate
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Synaptic dysfunction is an early event in Alzheimer's disease (AD) pathogenesis and directly related to cognitive impairment. 1 key finding →
Participants: 100 Evidence: low
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The CSF levels of Aβ42 but not total and phosphorylated tau were lower in APOE ε4 carriers compared with noncarriers irrespective of diagnostic group (cohort A). 3 key findings →
Participants: 105 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The cerebrospinal fluid (CSF) biochemical markers (biomarkers) Amyloidβ 42 (Aβ 42 ), total Tau (T-tau) and Tau phosphorylated at threonine 181 (P-tau 181 ) have proven diagnostic accuracy for mild cognitive impairment and dementia due to Alzheimer's Disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
CSF tau and 18 F-AV-1451 have equal performance in early clinical stages of AD, but 18 F-AV-1451 is superior in the dementia stage, and exhibits close to perfect diagnostic performance for mild to moderate AD. 3 key findings →
Participants: 14 Evidence: low
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The diagnostic guidelines of Alzheimer's disease (AD) have recently been updated to include brain imaging and cerebrospinal fluid (CSF) biomarkers, with the aim of increasing the certainty of whether a patient has an ongoing AD neuropathologic process or not. 3 key findings →
Design: cross-sectional Evidence: moderate
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Progressive cognitive decline in combination with a cerebrospinal fluid biomarker pattern of low levels of amyloid-β1-42 and high levels of total tau and phosphorylated tau is typical of Alzheimer's disease. 4 key findings →
Evidence: moderate
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A subgroup of patients with Alzheimer disease with extreme levels of CSF biomarkers exhibits worse clinical outcomes over time, including faster progression of cognitive deficits, no response to ChEI treatment, and a higher mortality. 1 key finding →
Participants: 151 Evidence: low
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Experimental studies suggest that the balance between short and long β-amyloid (Aβ) species might modulate the toxic effects of Aβ in Alzheimer disease (AD), but clinical evidence is lacking. 4 key findings →
Participants: 656 Evidence: moderate
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Changes in CSF biomarker levels may identify early neurodegenerative processes of Alzheimer disease. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Serine protease inhibitors (serpins), the acute phase reactants and regulators of the proteolytic processing of proteins, have been recognized as potential contributors to the pathogenesis of Alzheimer disease (AD). 4 key findings →
Participants: 258 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 32,180 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 32,180 records, built mostly from automated pulls of Europe PMC (66.5% of the library) and OpenAlex (15.8%), 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.
1,045 records (3.2% of the library) are not peer-reviewed — 966 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
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