27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
In the new AA diagnostic criteria, AD can be defined clinically as encompassing cognitively normal people having a core 1 AD biomarker. 5 key findings →
Evidence: low
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Twelve studies were identified. 2 key findings →
Design: systematic review Evidence: high
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Brazil's potential for dementia prevention is higher than in HIC. 1 key finding →
Design: longitudinal study Evidence: moderate
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Using exome sequencing, we identified a p.R191Q amino acid change in the valosin-containing protein (VCP) gene in an Italian family with autosomal dominantly inherited amyotrophic lateral sclerosis (ALS). 1 key finding →
Evidence: moderate
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Additionally, the performance of each scale to predict dementia pathology both individually and in combination was evaluated using a support vector classifier, which was compared with expert scan assessment to estimate clinical value. 2 key findings →
Participants: 184 Evidence: low
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Although dopamine replacement therapy remains a core component of Parkinson's disease treatment, the onset of motor fluctuations and dyskinetic movements might require a range of medical and surgical approaches from a multidisciplinary team, and important new approaches in the delivery of dopamine replacement are becoming available. 4 key findings →
Evidence: low
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Gut microbiota composition was associated with amyloid and p-tau status. 5 key findings →
Participants: 170 Evidence: moderate
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Our results demonstrate that different MAPT mutations give rise to distinct atrophy patterns and clinical phenotype, providing insights into the underlying disease biology and potential utility for patient stratification in therapeutic trials. 3 key findings →
Design: cohort study Evidence: moderate
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There was strong agreement regarding the definition of the core clinico-radiological syndrome, meaning that the current consensus statement should be regarded as a refinement, development, and extension of previous single-center PCA criteria rather than any wholesale alteration or redescription of the syndrome. 1 key finding →
Evidence: low
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Plasma markers of inflammation and complement dysregulation support diagnosis and outcome prediction in AD and MCI. 1 key finding →
Evidence: moderate
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Whether mild TBI (mTBI) in veterans confers a similar increased risk of AD is less known. 4 key findings →
Design: case-control study Participants: 51 Evidence: moderate
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The genetic variant rs72824905-G (minor allele) in the PLCG2 gene was previously associated with a reduced Alzheimer's disease risk (AD). 4 key findings →
Participants: 53,627 Evidence: low
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Plasma proteins affect biological processes and are common drug targets but their role in the development of Alzheimer's disease and related dementias remains unclear. 4 key findings →
Design: cohort study Evidence: moderate
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Our findings suggest a higher prevalence of Alzheimer’s disease dementia in older individuals and a lower prevalence of preclinical Alzheimer’s disease in younger groups than previously estimated 2 . 1 key finding →
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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The National Institute on Aging and the Alzheimer's Association charged a workgroup with the task of developing criteria for the symptomatic predementia phase of Alzheimer's disease (AD), referred to in this article as mild cognitive impairment due to AD. 5 key findings →
Evidence: low
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Despite continuing debate about the amyloid β-protein (or Aβ hypothesis, new lines of evidence from laboratories and clinics worldwide support the concept that an imbalance between production and clearance of Aβ42 and related Aβ peptides is a very early, often initiating factor in Alzheimer's disease (AD). 5 key findings →
Evidence: low
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Current criteria for the clinical diagnosis of pathologically confirmed corticobasal degeneration (CBD) no longer reflect the expanding understanding of this disease and its clinicopathologic correlations.
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It is not known exactly where amyloid-β (Aβ) fibrils begin to accumulate in individuals with Alzheimer's disease (AD).
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It was not possible to demonstrate significant differences on the co-primary clinical endpoints (ADAS-cog 11 and ADCS-ADL 23 ) at 52 weeks due to symptomatic activity in the control arm. 5 key findings →
Design: phase-3-trial Participants: 598 Evidence: null result
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A distinct set of midlife depressive symptoms was associated with an increased risk of dementia, suggesting that these symptoms might be early markers of underlying neurodegenerative processes. 4 key findings →
Design: cohort Participants: 5,811 Evidence: moderate
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The CSF Aβ42/Aβ40 and Aβ42/Aβ38 ratios are significantly better than CSF Aβ42 to detect brain amyloid deposition in prodromal AD and to differentiate AD dementia from non-AD dementias. 5 key findings →
Participants: 1,182 Evidence: low
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Elecsys-derived CSF biomarkers detect AD neuropathologic changes with very high discriminative accuracy in vivo. 2 key findings →
Participants: 27 Evidence: low
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It has been suggested that the diagnostic landscape of Alzheimer disease (AD) is undergoing a profound transformation, marked by a shift toward a biomarker-based approach, as proposed by the Revised Criteria for Diagnosis and Staging of Alzheimer's Disease. 2 key findings →
Design: longitudinal study Evidence: moderate
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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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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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →