27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Human genetic association studies point to immune response and lipid metabolism, in addition to amyloid-beta (Aβ) and tau, as major pathways in Alzheimer's disease (AD) etiology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Triggering receptor expressed on myeloid cells 2 (TREM2) homozygous mutations cause Nasu-Hakola disease, an early-onset recessive form of dementia preceded by bone cysts and fractures. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cancer mortality primarily stems from metastatic recurrence, emphasizing the urgent need for developing effective metastasis-targeted immunotherapies. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The association between dysfunctional microglia and amyloid-β (Aβ) is a fundamental pathological event and increases the speed of Alzheimer's disease (AD). 4 key findings →
Evidence: low
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Identification of multiple immune-related genetic risk factors for sporadic AD (sAD) have put the immune system center stage in mechanisms underlying this disorder. 4 key findings →
Evidence: low
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Variants of triggering receptor expressed on myeloid cells 2 (TREM2) are associated with an increased incidence of Alzheimer's disease, as well as other neurodegenerative disorders. 3 key findings →
Evidence: low
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Microglia-mediated neuroinflammation plays a crucial role in the pathogenesis of Parkinson's disease (PD). 4 key findings →
Evidence: low
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Microglia-mediated proteolysis of the triggering receptor expressed on myeloid cells-2 (TREM-2) produces soluble TREM-2 (sTREM-2) that can be measured in cerebrospinal fluid (CSF) samples. 4 key findings →
Participants: 59 Evidence: low
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Variations in many genes linked to sporadic Alzheimer's disease (AD) show abundant expression in microglia, but relationships among these genes remain largely elusive. 4 key findings →
Evidence: low
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Alzheimer's disease (AD) involves a dynamic interaction between neuroinflammation and metabolic dysregulation, where microglia play a central role. 4 key findings →
Evidence: low
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Late-onset Alzheimer's disease (AD; LOAD) is the most common human neurodegenerative disease, however, the availability and efficacy of disease-modifying interventions is severely lacking. 4 key findings →
Design: cross-sectional Evidence: low
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Alzheimer's disease (AD) is an age-related multifactorial neurodegenerative disorder. 4 key findings →
Participants: 26 Evidence: low
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Triggering receptor expressed on myeloid cells 2 (TREM2) is a single-pass transmembrane receptor of the immunoglobulin superfamily that is secreted in a soluble (sTREM2) form. 4 key findings →
Evidence: low
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Baseline tau-PET and a composite baseline cognitive score were the strongest independent predictors of cognitive decline. 4 key findings →
Evidence: low
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Mitochondrial DNA (mtDNA) variants associated with Alzheimer disease (AD) and Parkinson disease (PD) were sought by restriction endonuclease analysis in a cohort of 71 late-onset Caucasian patients. 4 key findings →
Evidence: moderate
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A genetic classification of Alzheimer disease(s) (AD) is presented. 4 key findings →
Evidence: low
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Familial Danish dementia (FDD), also known as heredopathia ophthalmo-oto-encephalica, is an autosomal dominant disorder characterized by cataracts, deafness, progressive ataxia, and dementia. 4 key findings →
Evidence: low
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In their study, Chen et al 1 examined the association between apolipoprotein E (APOE) genotype and longitudinal cognitive trajectories among middle-aged and older East Asian adults participating in the Healthy Aging Longitudinal Study of Taiwan (HALST).Although sporadic late-onset Alzheimer disease (AD) is polygenic, APOE remains the strongest genetic determinant of AD risk, with carriers of the APOE ε4 allele having increased odds of developing AD dementia in a dose-dependent manner compared with APOE ε3 homozygotes. 1 key finding →
Design: longitudinal study Participants: 21 Evidence: moderate
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Dementia, particularly Alzheimer's disease (AD), presents a growing global health challenge characterized by cognitive decline, behavioral changes, and loss of independence. 1 key finding →
Participants: 2,878 Evidence: moderate
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Tau accumulates in a group of neurodegenerative diseases known as tauopathies. 1 key finding →
Evidence: low
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The Dominantly Inherited Alzheimer Network Observational Study (DIAN Obs) is a longitudinal, global cohort study investigating brain aging and autosomal dominant Alzheimer’s disease (ADAD), a rare monogenic form of Alzheimer’s disease (AD). 5 key findings →
Design: cohort study Evidence: moderate
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Genome-wide association studies have led to numerous genetic loci associated with Alzheimer's disease (AD). 1 key finding →
Participants: 2,247 Evidence: low
Full summary, score breakdown and related studies → Original source
A total of 12 studies were included, with overall moderate risk of bias, mainly due to inadequate randomization and blinding. 3 key findings →
Design: systematic review Participants: 12 Evidence: high
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This review substantiates the evolving understanding of TREM2's disease progression-dependent impacts. 1 key finding →
Design: systematic review Participants: 43 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Recent studies show that heterozygous variant of triggering receptor expressed on myeloid cells 2 (TREM2) increase the risk of Alzheimer's disease (AD) but with inconclusive results. 3 key findings →
Design: meta-analysis Evidence: high
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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 27,380 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 →