28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Study objectives To investigate the cumulative effect of five consecutive nights of partial sleep deprivation (PSD) on a panel of cerebrospinal fluid (CSF) biomarkers in healthy adults. 1 key finding →
Participants: 13 Evidence: high
Full summary, score breakdown and related studies → Original source
These results suggest that increasing levels of tau most consistently relate to declines in cognition preceding biomarker collection. 4 key findings →
Design: longitudinal study Participants: 152 Evidence: moderate
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Baseline biomarkers largely do not predict risk for developing ARIA-E. ARIA-E was associated with significant longitudinal changes in several biomarkers, with larger reductions in amyloid PET and CSF p-tau and t-tau concentrations, and paradoxically greater hippocampal volume reduction and ventricular enlargement, suggesting that ARIA-E in bapineuzumab-treated cases may be related to increased Aβ efflux from the brain and affecting downstream pathogenic processes. 4 key findings →
Design: longitudinal study Participants: 1,512 Evidence: moderate
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Serum NFL is increased in ALS in comparison to other conditions and can serve as diagnostic and prognostic biomarker. 2 key findings →
Design: longitudinal study Participants: 124 Evidence: moderate
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Inclusion criteria included clinical diagnosis of PPA; availability of complete speech, language, and cognitive testing; magnetic resonance imaging performed within 6 months of the cognitive evaluation; and PET carbon 11-labeled Pittsburgh Compound-B or florbetapir F 18 brain scan results. 5 key findings →
Design: longitudinal study Participants: 109 Evidence: moderate
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Future research should examine whether minimizing drawbacks at the pre-imaging stage has adverse consequences on results disclosure. 5 key findings →
Design: randomized controlled trial Participants: 59 Evidence: high
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The diagnostic performance of plasma biomarkers was poor (area under the curve [AUC] between 0·53 [95% CI 0·44-0·62] and 0·74 [0·66-0·82]) except for plasma NfL concentrations, which had an AUC of 0·88 (0·82-0·93) for the differentiation of the asymptomatic group versus the prodromal Alzheimer's disease group and 0·95 (0·92-0·98) for the asymptomatic group versus the Alzheimer's disease dementia group. 4 key findings →
Design: cross-sectional Participants: 282 Evidence: low
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Of the reference regions used, subcortical white matter, cerebellar white matter, and the pons, alone or in combination, generated the largest effect sizes. 5 key findings →
Evidence: high
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These analyses provide preliminary support for IICV as a marker of incident AD and MCI. 4 key findings →
Design: longitudinal study Participants: 105 Evidence: moderate
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Inner retina in Alzheimer's Disease (AD) may experience neuroinflammation resulting in atrophy. 3 key findings →
Design: case-control study Participants: 15 Evidence: moderate
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We developed, replicated, and validated an MRI measure of cerebrovascular and neurodegenerative pathologies that are associated with clinical and neuropathologic diagnosis of AD and related to established biomarkers. 5 key findings →
Design: cross-sectional Participants: 1,175 Evidence: moderate
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This study demonstrated the measurement of high-performance plasma amyloid-β biomarkers by immunoprecipitation coupled with mass spectrometry to predict individual brain amyloid-β status as determined by amyloid-β-PET imaging. 4 key findings →
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NF-L is a biomarker for neurodegeneration in DS with potential for use in future clinical trials to prevent or delay dementia. 2 key findings →
Design: cross-sectional Participants: 100 Evidence: moderate
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Levels of plasma Aβ42 and Aβ42/Aβ40 ratio were elevated in patients with possible cognitive impairment, indicating that plasma Aβ42 and Aβ42/Aβ40 ratio increases may be more pronounced in early stage of cognitive impairment. 2 key findings →
Design: cross-sectional Participants: 1,314 Evidence: low
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Amyloid PET results were positive for 242 patients (48%). 4 key findings →
Participants: 866 Evidence: moderate
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This study reviewed the structure, function, analytical aspects, and age-dependent normal ranges of neurofilaments, providing a comprehensive overview of neurofilament light chain as a marker of axonal injury across various neurological disorders. 2 key findings →
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NfL and p/t-tau similarly discriminated FTD from controls, but not between clinical subtypes, apart from FTD-MND. 2 key findings →
Participants: 361 Evidence: moderate
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We found increased levels of YKL-40 and decreased levels of sAPPβ in both FTD and ALS groups compared to controls. 2 key findings →
Design: cross-sectional Participants: 86 Evidence: low
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These results provide evidence that, in the absence of significant neurodegenerative processes, individuals who harbor AD neuropathology may remain cognitively unimpaired. 4 key findings →
Design: cross-sectional Participants: 79 Evidence: low
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These longitudinal estimates clarify the sequence and temporal dynamics of presymptomatic pathologic changes in autosomal dominant AD, information critical to a better understanding of the disease. 3 key findings →
Design: cross-sectional Evidence: moderate
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Plasma a-synuclein level was significantly increased in patients with PD and APS when compared with controls and FTD without parkinsonism (p<0.01). 5 key findings →
Participants: 204 Evidence: low
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As serum NfL correlates with functional impairment and brain atrophy in bvFTD at different disease stages, we propose it as marker of disease severity, paving the way for its future use as outcome measure for clinical trials. 1 key finding →
Participants: 74 Evidence: low
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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
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
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Nine hundred and four participants (342 AD and 562 NAD) were studied; 400 in Mtp-1 and 504 in Mtp-2. 5 key findings →
Participants: 904 Evidence: low
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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 →