31,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Among the plasma biomarkers, phosphorylated tau (p-tau) 217 exhibited the highest concordance rate with Aβ (2326 of 2571 [90.5%]) and tau (100 of 120 [83.3%]) PET. 4 key findings →
Design: cohort study Participants: 2,611 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Greater neighborhood disadvantage was associated with elevated inflammatory and AD CSF biomarkers cross-sectionally and longitudinal increases in a nonspecific inflammatory blood biomarker. 5 key findings →
Design: longitudinal study Participants: 334 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The relationship between sensory impairment and cognitive impairment was not unique to one sensory system, suggesting that sensorineural health may be a marker of brain aging. 2 key findings →
Design: longitudinal study Participants: 1,884 Evidence: moderate
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Understanding how metabolites are longitudinally influenced by age and sex could facilitate the identification of metabolomic profiles and trajectories that indicate disease risk. 4 key findings →
Design: longitudinal study Participants: 1,212 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The temporal evolutions and relative orderings of Alzheimer disease biomarkers, including CSF amyloid-β42 (Aβ42), Aβ40, total tau (Tau) and phosphorylated tau181 (pTau181), standardized uptake value ratio (SUVR) from the molecular imaging of cerebral fibrillar amyloid-β with PET using the 11C-Pittsburgh Compound-B (PiB), MRI-based hippocampal volume and cortical thickness and cognition have been hypothesized but not yet fully tested with longitudinal data for all major biomarker modalities among cognitively normal individuals across the adult lifespan starting from 18 years. 4 key findings →
Design: longitudinal study Participants: 2,609 Evidence: moderate
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This longitudinal study examined whether insulin resistance among late middle-aged, cognitively healthy individuals was associated with 1) less gray matter in Alzheimer disease-sensitive brain regions and 2) worse cognitive performance. 4 key findings →
Design: longitudinal study Participants: 372 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Higher levels of P-tau181 (HR = 1.32 [95% CI: 1.17-1.51]), NfL (HR = 1.19 [95% CI: 1.03-1.36]), and GFAP (HR = 1.36 [95% CI: 1.22-1.52]), and a lower Aβ42/Aβ40 ratio (HR = 0.80 [95% CI: 0.68-0.95]) were associated with an increased risk of progressing to clinically-diagnosed DAT. 2 key findings →
Design: longitudinal study Participants: 1,007 Evidence: moderate
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The sample included 4340 adults (mean [SD; range] age, 58.1 [1.1; 56-63] years; 2400 [55.3%] women); 630 (14.4%) were Black, 900 (20.7%) were Latinx, and 2610 (60.1%) were White. 5 key findings →
Design: cohort study Participants: 4,340 Evidence: moderate
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Mean annual costs for individuals with clinically diagnosed AD were SEK 99,906, SEK 290,972, SEK 479,524, and SEK 795,617 in mild cognitive impairment (MCI), mild, moderate, and severe AD. 1 key finding →
Design: cohort Participants: 95,853 Evidence: high
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Adults with Down syndrome demonstrate striatum-first amyloid accumulation with [ 11 C]PiB PET imaging, which has not been replicated with [ 18 F]florbetapir (FBP). 4 key findings →
Design: longitudinal study Participants: 175 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A total of 807 K-ROAD participants (median age 72.0 years, 58.7% female) and 230 ADNI participants (median age 70.9 years, 49.1% female) were analyzed. 5 key findings →
Design: cohort study Participants: 807 Evidence: moderate
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Comorbid cardiovascular and metabolic risk factors (CVM) differentially impact brain structure and increase dementia risk, but their specific magnetic resonance imaging signatures (MRI) remain poorly characterized. 1 key finding →
Design: cohort study Participants: 37,096 Evidence: moderate
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These findings suggest amyloid pathologies significantly influence white matter and that these abnormalities may signify an early feature of the disease process. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These findings suggest that increases in certain plasma AD biomarkers are associated with NP in WLWH and WLWOH and may be associated with later onset of AD, and measuring these biomarkers could be a pivotal advancement in monitoring aging brain health and development of AD among women with and without HIV. 5 key findings →
Design: cohort study Participants: 307 Evidence: moderate
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Among adults with Down syndrome, the striatum consistently accumulates amyloid earlier than the cortex when measured with PiB. 2 key findings →
Design: longitudinal study Participants: 175 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Microglia activation is the brain's major immune response to amyloid plaques in Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We investigated the effects of matrix type and reagent batch changes on diagnostic performances and longitudinal trajectories of brain-derived tau (BD-tau). 4 key findings →
Design: longitudinal study Participants: 26 Evidence: moderate
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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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The sample included 740 donors (417 female [56.4%]; mean [SD] age at death, 81.5 [10.3] years; mean [SD] VBI score, 0.7 [1.0]; and median life course ADI, 7.08 [IQR, 4.33-9.83]), with residential years spanning 1905 to 2018. 5 key findings →
Design: cohort study Participants: 740 Evidence: moderate
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Plasma p-tau217 concentrations, considered together with APOE genotype, might help stratify risk and estimate the timing of future cognitive impairment in asymptomatic individuals who are at increased risk for Alzheimer's disease, such as those with a family history of dementia or known APOE-ε4 carrier status. 5 key findings →
Design: cohort Participants: 8,582 Evidence: high
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Plasma β-synuclein demonstrated discriminative properties for Aβ PET positive and negative subjects. 3 key findings →
Design: longitudinal study Participants: 51 Evidence: moderate
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A biological research framework to define Alzheimer' disease with dichotomized biomarker measurement was proposed by National Institute on Aging-Alzheimer's Association (NIA-AA). 3 key findings →
Design: longitudinal study Evidence: moderate
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Changes to everyday spoken language ("connected language") are evident in persons with AD dementia, yet little is known about when these changes are first detectable on the continuum of cognitive decline. 2 key findings →
Design: longitudinal study Participants: 264 Evidence: moderate
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These results suggest that all adults with Down syndrome should be screened for Alzheimer's disease pathology starting shortly before age 40 years and considered for clinical trials. 1 key finding →
Design: longitudinal study Participants: 328 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A total of 1,345 individuals were included. 5 key findings →
Design: cohort study Participants: 1,345 Evidence: moderate
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 31,780 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.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 31,780 records, built mostly from automated pulls of Europe PMC (66% of the library) and OpenAlex (16%), 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 (3.3% 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 →
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