28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Human leukocyte antigen (HLA) class II variation is implicated in Alzheimers disease (AD) and longevity, but its mechanisms within the major histocompatibility complex remain unclear. 2 key findings →
Participants: 6,053 Evidence: moderate
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Neuropsychiatric symptoms (NPS) are increasingly recognized as critical components of the disease progression in Alzheimers disease (AD), yet their relationship with neurodegeneration remain poorly characterized. 2 key findings →
Participants: 1,756 Evidence: low
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Polygenic and proteomic risk scores are both proposed for pre-symptomatic stratification, yet the extent to which they provide overlapping or complementary information has not been measured across neurodegenerative disease. 3 key findings →
Evidence: moderate
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Genome-wide genotypes were quality-controlled, imputed, functionally annotated (yielding 16,935 gene regions comprising 90,607 functional variants), and associated with latent EEG features using Bayesian reduced rank regression. 5 key findings →
Evidence: low
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Impairment in the comprehension of morphosyntactic and transitivity information does not feature in current diagnostic guidelines for primary progressive aphasia (PPA) or Alzheimers Diseases (AD), despite research reporting delayed sensitivity or insensitivity of these clinical populations to these linguistic domains. 2 key findings →
Evidence: low
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BackgroundThe Centiloid (CL) scale standardizes global amyloid PET quantification and is widely used to define amyloid positivity. 5 key findings →
Design: meta-analysis Participants: 71 Evidence: high
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BackgroundFluid biomarkers enable the demonstration of the biological effects of novel therapies in Alzheimers disease (AD). 1 key finding →
Design: longitudinal study Participants: 65 Evidence: high
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The purpose of this meta-analysis was to determine the common signature of dysregulated brain glucose metabolism in late-onset age-associated neurodegenerative diseases (A2NDs), including Alzheimer disease, Parkinson disease, and amyotrophic lateral sclerosis. 2 key findings →
Design: meta-analysis Participants: 5,298 Evidence: high
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Understanding how the contents of consciousness, particularly perceptual awareness, change with the progression of AD is crucial for meaningful person-centred care. 4 key findings →
Evidence: low
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INTRODUCTIONBiomarkers for monitoring disease activity and treatment response in peripheral neuropathies remain limited. 3 key findings →
Participants: 81 Evidence: low
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Early identification of Alzheimers disease and related dementias (ADRD) remains challenging despite its importance for timely intervention, management of modifiable risk factors, and care planning. 2 key findings →
Design: longitudinal study Evidence: moderate
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Dopamine replacement therapy (DRT) alleviates motor symptoms in Parkinsons disease (PD) but can trigger hallucinations in a subset of patients, yet the neural basis of this selective vulnerability is unknown. 1 key finding →
Evidence: low
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BackgroundUnderstanding the mechanisms underlying brain aging and age-related pathological changes is essential for advancing brain health research. 3 key findings →
Participants: 211 Evidence: moderate
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Service members with traumatic brain injury are at approximately two- to four-fold higher risk of Alzheimers disease or related dementias than those without such an injury, with risk increasing with injury severity. 5 key findings →
Participants: 57 Evidence: moderate
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BackgroundPhenotypic age acceleration (PhenoAgeAccel), derived from PhenoAge, and MetaboHealth are composite exposures of biological ageing and metabolic health associated with dementia-related outcomes. 4 key findings →
Design: longitudinal study Participants: 272 Evidence: moderate
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Multi-trait QTL (xQTL) colocalization has shown great promises in identifying causal variants with shared genetic etiology across multiple molecular modalities, contexts, and complex diseases. 2 key findings →
Participants: 595 Evidence: low
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INTRODUCTIONMultimodal biomarkers have transformed Alzheimers disease research, but the incremental contribution of each modality to predicting progression from mild cognitive impairment (MCI) remains unclear. 3 key findings →
Participants: 2,430 Evidence: low
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BackgroundThe prevalence and pattern of secondary causes of first-onset psychosis (FEP) in Asian populations are understudied. 2 key findings →
Participants: 37 Evidence: moderate
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ObjectiveRegression-based normative approaches are widely used in neuropsychology but often rely on score transformations to satisfy model assumptions. 1 key finding →
Participants: 131 Evidence: moderate
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BackgroundAccurate prediction of progression from mild cognitive impairment (MCI) to Alzheimers disease (AD) is important for prognosis, patient management, and clinical trial enrollment. 5 key findings →
Participants: 2,430 Evidence: low
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INTRODUCTIONAPOE*{varepsilon}4 is the strongest genetic risk factor for Alzheimers disease (AD), yet its effect varies across ancestral populations. 1 key finding →
Participants: 2,733 Evidence: low
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BackgroundFear of dementia (FoD) can shape psychological well-being and responses to perceived cognitive change. 5 key findings →
Evidence: low
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O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=113 SRC="FIGDIR/small/26361997v1_ufig1.gif" ALT="Figure 1"> View larger version (32K): org.highwire.dtl.DTLVardef@1dac0d9org.highwire.dtl.DTLVardef@aaf8f2org.highwire.dtl.DTLVardef@be10a1org.highwire.dtl.DTLVardef@35c7be_HPS_FORMAT_FIGEXP M_FIG C_FIG BACKGROUNDThe effect of neurovascular health on cardiovascular outcomes is not well-known. 4 key findings →
Participants: 3,263 Evidence: moderate
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IntroductionPolygenic risk scores (PRS) may improve Alzheimers disease (AD) risk prediction before symptom onset, yet choosing an appropriate model can be challenging. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The Middle East and North Africa (MENA) region is projected to experience the fastest growth in dementia burden globally, yet population-based data on cognitive aging remain scarce. 1 key finding →
Participants: 3,027 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.
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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →