28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Neurofilament light chain (NfL) is an axonal protein that when measured in cerebrospinal fluid (CSF) serves as a biomarker of neurodegeneration. 3 key findings →
Participants: 278 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The score reflecting the severity of Aβ pathology showed a better correlation with ln(Aβ42/Aβ40) (R 2 = 0.506, β = -0.713, P < 0.001) than with ln(Aβ42) (R 2 = 0.206, β = -0.458, P < 0.001), which was confirmed after adjusting for covariates. 4 key findings →
Participants: 159 Evidence: low
Full summary, score breakdown and related studies → Original source
SerpinA1 (α1-antitrypsin) is a soluble glycoprotein, the cerebrospinal fluid (CSF) isoforms of which showed disease-specific changes in neurodegenerative disorders that are still unexplored in Alz-heimer’s disease (AD). 3 key findings →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source
We aimed to assess the utility of AT(N) classification in clinical practice. 2 key findings →
Participants: 230 Evidence: low
Full summary, score breakdown and related studies → Original source
This study aimed to investigate the interaction between weight loss (WL) and plasma amyloid-β 42/40 (Aβ 42/40), neurofilament light chain (NfL), progranulin, and their association with cognitive decline over time among older adults. 4 key findings →
Participants: 470 Evidence: low
Full summary, score breakdown and related studies → Original source
Comorbid Alzheimer's disease (AD) neuropathology is common in Lewy body disease (LBD); however, AD comorbidity in the prodromal phase of LBD remains unclear. 2 key findings →
Participants: 84 Evidence: moderate
Full summary, score breakdown and related studies → Original source
AD-MCI and AD-DEM patients showed increased p-tau217 and spectral slowing (higher theta, lower alpha). 4 key findings →
Participants: 128 Evidence: low
Full summary, score breakdown and related studies → Original source
Glial fibrillary acidic protein (GFAP) and neurofilament light (NfL) are putative non-amyloid biomarkers indicative of ongoing inflammatory and neurodegenerative disease processes. 2 key findings →
Participants: 20 Evidence: moderate
Full summary, score breakdown and related studies → Original source
After adjustment, only plasma p‐tau181 and NfL were significantly elevated in Aβ+ Obj‐SCD participants compared to Aβ− NC group. 5 key findings →
Participants: 234 Evidence: low
Full summary, score breakdown and related studies → Original source
The determination of cut-off points of core AD CSF biomarkers for the participating centers allows a better diagnostic accuracy. 1 key finding →
Participants: 42 Evidence: low
Full summary, score breakdown and related studies → Original source
In this real-world dataset, we identified effects of multimorbidities on plasma biomarkers, especially kidney function. 2 key findings →
Design: cross-sectional Participants: 617 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Glial fibrillary acidic protein (GFAP) is the main astrocytic intermediate filament (IF). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We observed good convergence among the 4 Good convergence was obtained among several methods for determining an optimal cutoff for 18 F-AZD4694 PET positivity. 3 key findings →
Participants: 22 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Plasma GFAP effectively distinguished AD dementia from multiple neurodegenerative diseases, gradually increased across the AD continuum, predicted the individual risk of AD progression, and strongly correlated with AD CSF/neuroimaging biomarkers. 2 key findings →
Participants: 818 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The extent to which Alzheimer neuropathology, particularly the accumulation of misfolded beta-amyloid, contributes to cognitive decline and dementia in Parkinson's disease (PD) is unresolved. 1 key finding →
Design: cross-sectional Participants: 23 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Higher grey matter volumes/cortical thickness and fluorodeoxyglucose uptake have been consistently found in cognitively unimpaired individuals with abnormal Alzheimer's disease biomarkers compared with those with normal biomarkers. 4 key findings →
Participants: 319 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
MR analysis suggested a causal relationship between decreased blood-derived mtDNA-CN and increased risk of AD (OR = 0.68; P = 0.013). 5 key findings →
Participants: 13,799 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Increased concentrations of baseline plasma t-tau may predict in vivo structural BFCS atrophy progression in older adults at risk for AD, independently of β-amyloid status and APOE genotype. 3 key findings →
Participants: 251 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The combination of amyloid and tau PETs was associated with changes in management and diagnosis of MCI and dementia, and the second-generation tau PET has a strong impact on the changes in diagnosis and management in memory clinics. 5 key findings →
Participants: 40 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The HCTS pattern represents a definable subgroup of non-AD pathophysiology (i.e., T - [N] + ) that is associated with cognitive impairment. 2 key findings →
Participants: 684 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Of 108 participants (age: 69 ± 6.5 years; 54.6% female) with paired samples obtained at time of LP, 64.8% (n = 70/108) had Aβ pathology detected (35 with Mild Cognitive Impairment and 35 with mild dementia). 2 key findings →
Participants: 70 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Neither fibrillar nor nonfibrillar Aβ content alone sufficed to explain the Aβ PET findings in either AD model. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Tau IQ successfully calculated global tau load (Tau L ) in all 791 scans analyzed (range, -3.5% to 185.2%; mean ± SD, 23% ± 20.5%) with a nonzero additional local tau component being required in 31% of all scans (cognitively normal [CN], 22%; mild cognitive impairment [MCI], 35%; dementia, 72%). 5 key findings →
Design: cross-sectional Participants: 615 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This study suggests that the baseline value of amyloid PET and CSF Aβ 42 measures may be useful for screening participants for AD trials; however, brain hippocampus atrophy and hypometabolism are only useful as repeated longitudinal assessments for tracking cognition and disease progression. 3 key findings →
Design: longitudinal study Participants: 262 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Higher sNfL concentrations were associated with worse performance in cognitive tests at baseline, including CERAD (B = −10.084, SE = 2.999, p < 0.001) and MMSE (B = −3.014, SE = 1.293, p = 0.021). 3 key findings →
Design: cross-sectional Participants: 237 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 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 →