27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
We quantified glial fibrillary acidic protein (GFAP) using immunoblot techniques and anti-GFAP, in unfractionated homogenates of different brain regions from Alzheimer's disease (AD) patients. 1 key finding →
Evidence: low
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The findings provide further in vivo evidence that astrocytosis occurs early in AD, preceding Aβ plaque deposition. 5 key findings →
Evidence: low
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Hippocampal atrophy and amyloid deposition seem to dissociate during the evolution of MCI, the atrophy increasing clearly and [(11)C] PiB retention changing modestly when conversion to AD occurs. 4 key findings →
Evidence: low
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The results for both (11)C-PiB and (18)F-NAV4694 can now be expressed in centiloids, an important step that should allow better clinical and research use of Aβ imaging. 3 key findings →
Evidence: low
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Exposure to air pollutants, including particulate matter, results in activation of the brain inflammatory response and Alzheimer disease (AD)-like pathology in dogs and humans. 1 key finding →
Evidence: low
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These results suggest that 4-O-methylhonokiol inhibits LPS-induced amyloidogenesis via anti-inflammatory mechanisms. 3 key findings →
Evidence: low
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Chronic neuroinflammation is a hallmark of the onset and progression of brain proteinopathies such as Alzheimer disease (AD) and it is suspected to participate in the neurodegenerative process. 1 key finding →
Evidence: low
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Amyloid PET imaging is a novel diagnostic test that can detect in living humans one of the two defining pathologic lesions of Alzheimer disease, amyloid-β deposition in the brain. 3 key findings →
Evidence: low
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In younger controls, SUV peak was observed in the temporal lobe with values of approximately 3.0 for 11 C-RO-963, 1.5 for 11 C-RO-643, and 3.5 for 18 F-RO-948. 5 key findings →
Evidence: low
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Although clinical routine focuses on dichotomous and visual interpretation of amyloid PET, regional image assessment in research settings may yield additional opportunities. 5 key findings →
Design: cross-sectional Evidence: moderate
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They also suggest that FW elevation occurs in the locus coeruleus to transentorhinal cortex tract, nucleus basalis of Meynert, and hippocampus in the transition from CN to EMCI, while other basal forebrain regions and the entorhinal cortex are not affected until a later stage of AD. 2 key findings →
Evidence: low
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These results show significant differences in neurogranin and total-tau between typical and atypical patients, which may relate to factors other than disease topography. 4 key findings →
Participants: 27 Evidence: low
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Elevated microglial activation in the right amygdala-entorhinal-hippocampal complex of App NL-G-F mice is associated with better spatial learning. 5 key findings →
Design: cross-sectional Evidence: low
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We hypothesize the population without dementia can be subdivided into participants with and without biological Alzheimer disease (AD) based on the combination of CSF Aβ42 and p-tau/t-tau (represented also by the p-tau/t-tau/Aβ42 ratio). 5 key findings →
Participants: 547 Evidence: low
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Plasma p-tau-181 and GFAP are closely associated with synaptic density measured using 18 F-SynVesT-1 PET/MRI, with the relationship primarily influenced by tau accumulation rather than Aβ deposition or cortical thickness. © RSNA, 2024 Supplemental material is available for this article. 2 key findings →
Participants: 50 Evidence: low
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The progressive decrement of neuropsychological performance is associated with HVL long before the emergence of clinically overt symptoms. 4 key findings →
Design: longitudinal study Evidence: moderate
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MMSE score showed a positive correlation with the Aβ 1-42 concentrations ( r = 0.485; p r = -0.418; p = 0.002). 5 key findings →
Design: cross-sectional Evidence: moderate
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Our findings suggest AD-type tau is not higher in LLD compared to non-depressed, cognitively unimpaired older adults and appears unlikely to contribute to lower gray matter volume in LLD, further underscoring the need to distinguish major depressive disorder from depressive symptoms occurring in early AD. 5 key findings →
Design: cross-sectional Participants: 102 Evidence: low
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ε4, socioeconomic status, physical activity, smoking, subjective cognitive decline, and various cardiovascular risk factors and comorbidities. 4 key findings →
Design: cross-sectional Evidence: moderate
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The Centiloid method demonstrates strong intertracer and interscanner harmonization when standardized to the 11C-Pittsburgh compound B reference, with high correlation (r2 > 0.9) across 18F-labeled tracers, including florbetapir, flutemetamol, and florbetaben. 5 key findings →
Design: longitudinal study Evidence: moderate
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Reduction in CSF Abeta(42), likely reflecting Abeta aggregation in the brain, is associated with brain atrophy in the preclinical phase of AD. 3 key findings →
Participants: 29 Evidence: low
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The same tube type should be used in research studies on blood biomarkers. 2 key findings →
Evidence: low
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Clinical prediction models combining plasma biomarkers-particularly p-tau217-exhibit high performance and are less effected by random error. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
These results suggest that persons carrying certain genotypes in IL10 (-1082G/A), IL1β (1473C/G), IL6 (-174C/G), and TNFIα (-308A/G) could be more vulnerable to development of neuroinflammation, and consequently of AD. 2 key findings →
Participants: 115 Evidence: low
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Plasma P-tau181 effectively detects Aβ+ status and conversion to dementia, confirming the value of this blood biomarker for the management of AD. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →