27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Regions with early signs of elevated amyloid β uptake were used to form an early, focal composite and compared to a commonly used global composite, in a separate validation sample. 3 key findings →
Design: longitudinal study Participants: 279 Evidence: moderate
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Although recent studies have demonstrated the prognostic utility of plasma biomarkers of Alzheimer pathology or neurodegeneration, such as pTau-181 and NF-L, whether other plasma biomarkers can further improve prediction of cognitive decline is undetermined. 5 key findings →
Design: cohort study Participants: 60 Evidence: moderate
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Sleep abnormalities are prevalent in Alzheimer's disease, with sleep quality already impaired at its preclinical stage. 4 key findings →
Design: cohort study Participants: 1,168 Evidence: moderate
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NEFL (hazard ratio [HR] [95% confidence intervals (CIs)]: 1.54 [1.29, 1.84]) and RPS6KB1 (HR [95% CI]: 1.33 [1.16, 1.52]) were robustly associated with incident all-cause dementia; MMP12 (HR [95% CI]: 2.06 [1.41, 2.99]) was associated with vascular dementia in ELSA, after correcting for multiple testing. 3 key findings →
Design: longitudinal study Participants: 3,249 Evidence: moderate
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Although, anatomical disparities of the rodent medial prefrontal cortex compared to the primate homologue are apparent, current rodent models have effectively implicated the medial prefrontal cortex as a neural substrate of cognitive decline within ageing and dementia. 4 key findings →
Design: cross-sectional Evidence: moderate
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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
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For amyloid positive individuals Aβ42/Aβ40, glial fibrillary acidic protein and p-tau181 were the top predictors of cognitive decline while Aβ42/Aβ40 was prominent for amyloid negative participants across all age groups. 5 key findings →
Design: cross-sectional Participants: 1,185 Evidence: moderate
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Apathy is a prevalent and persistent neuropsychiatric syndrome across many neurological disorders, significantly impacting both patients and caregivers. 4 key findings →
Participants: 335 Evidence: low
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In the last few years, co-ultramicronized palmitoylethanolamide combined with luteoline has emerged as a potential therapeutic molecule in neurodegenerative disorders pathogenically related to frontotemporal dementia, for its demonstrated strong anti-inflammatory and neuroprotective properties. 4 key findings →
Design: clinical trial Participants: 25 Evidence: high
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Clinical Dementia Rating-Global scores (1.44 ± 0.65 versus 0.24 ± 0.25; P < 0.0001) and Patient Health Questionnaire-9 scores (4.88 ± 4.21 versus 0.20 ± 0.50; P < 0.0001) were higher than controls. 4 key findings →
Design: cross-sectional Participants: 25 Evidence: moderate
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The results demonstrate that, although the number of biomarkers has rapidly expanded, many are interrelated and few strongly predict clinical outcomes. 1 key finding →
Design: cross-sectional Evidence: moderate
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Genome-wide association studies of late-onset Alzheimer's disease risk have previously identified genes primarily expressed in microglia that form a transcriptional network. 4 key findings →
Evidence: low
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Our results pertaining to menopause-related characteristics, such as age at menopause or menopause hormonal therapy, did not replicate the literature reporting an association with WMH volumes. 5 key findings →
Design: cross-sectional Participants: 9,560 Evidence: low
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Having three or more vascular risk factors (odds ratio = 1.23, 95% confidence interval [1.04-1.47]), actively smoking (odds ratio = 1.54, 95% confidence interval [1.29-1.82]), being overweight (odds ratio = 1.46, 95% confidence interval [1.22-1.74]), and having diabetes (odds ratio = 1.29, 95% confidence interval [1.09-1.53]) were associated with higher odds of subjective cognitive decline. 2 key findings →
Design: cross-sectional Evidence: low
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Lewy body patients showed a significantly higher degree of WMSA in the external capsule cholinergic pathway despite no significant differences in global WMSA compared to controls. 4 key findings →
Participants: 82 Evidence: moderate
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Alzheimer's disease (AD) and vascular dementia (VaD) exhibit distinct neuropathological hallmarks, with AD defined by cortical amyloid plaques and neurofibrillary tangles, while VaD arises primarily from cerebrovascular disease (CeVD). 4 key findings →
Participants: 531 Evidence: moderate
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Alzheimer's disease is associated with pre-symptomatic changes in brain morphometry and accumulation of abnormal tau and amyloid-beta pathology. 4 key findings →
Design: cross-sectional Evidence: moderate
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Moreover, a theoretical model proposes that frontotemporal dementia manifestations result from a deficit in goal-directed behaviour, which may be related to altered dopamine control of the frontostriatal circuitry. 4 key findings →
Participants: 139 Evidence: low
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The number of people living with dementia worldwide is projected to reach 150 million by 2050, making prevention a crucial priority for health services. 3 key findings →
Participants: 712 Evidence: low
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Higher scores in cognitive screening [odds ratio (OR): 1.23], facial emotion processing (OR: 1.69), episodic memory (OR: 1.09), animal fluency (OR: 1.17), working memory (OR: 1.18), letter fluency (OR: 1.17) and depressive symptoms (OR: 7.41) were significantly associated with PPD (all Ps ≤ 0.010). 2 key findings →
Evidence: low
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The study population demonstrated limited PET-based amyloid-β and tau pathology, which did not associate with any of the investigated plasma biomarkers. 5 key findings →
Design: cross-sectional Participants: 49 Evidence: low
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These findings suggest that subcortical VCIND modifies the relationship between FPN lateralization and cognitive functions, rather than altering the lateralization pattern itself. 1 key finding →
Participants: 30 Evidence: high
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These findings support the interpretation that acute rises in CSF NfL concentration are likely to be related to passive release or CSF clearance failure. 1 key finding →
Evidence: moderate
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None of the genetically proxied functional network features were significantly associated with neurodegenerative outcomes (adjusted P value >0.05), despite sufficient calculated power. 5 key findings →
Participants: 47 Evidence: low
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Finally, we showed that the MD-MRI-derived astrogliosis biomarker is the only MRI measure capable of predicting cognitive state. 5 key findings →
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.
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 →