27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The aim of this study was to provide an update on the role of the innate immune system and neuroinflammation in the pathogenesis of Alzheimer's disease, with an emphasis on microglial receptors CD33 and TREM2. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Upon demyelinating injury, microglia orchestrate a regenerative response that promotes myelin repair, thereby restoring rapid signal propagation and protecting axons from further damage. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) and dementia in general are age-related diseases with multiple contributing factors, including brain inflammation. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer's disease (AD) neuropathology is associated with neuroinflammation, but there are few useful biomarkers. 4 key findings →
Participants: 100 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
While macrophage heterogeneity during metabolic dysfunction-associated steatohepatitis (MASH) has been described, the fate of these macrophages during MASH regression is poorly understood. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Neurodegenerative disorders, including Alzheimer's disease, are associated with microgliosis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Triggering receptor expressed on myeloid cells 2 (Trem2) is a myeloid cell-specific gene expressed in brain microglia, with variants that are associated with neurodegenerative diseases, including Alzheimer's disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Lung macrophages play a pivotal role in pulmonary fibrosis, with monocyte-derived alveolar macrophages driving disease progression. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Activation of microglia, the resident immune cells of the central nervous system, is a prominent pathological hallmark of Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Many genetic studies for Alzheimer's disease (AD) have been focused on the identification of common genetic variants associated with AD risk and not on other aspects of the disease, such as age at onset or rate of dementia progression. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Late-onset Alzheimer's disease (LOAD) is the most common form of dementia worldwide. 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In a previous study of normal elderly male twins, the heritability of quantitative white matter hyperintensity (WMH) volume has been estimated to be high (0.73). 4 key findings →
Participants: 2,012 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer's disease (AD) is the most frequently occurring type of dementia. 4 key findings →
Participants: 483,507 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Recent studies suggest that plasma phosphorylated tau181 (p-tau181) is a highly specific biomarker for Alzheimer's disease (AD)-related tau pathology. 4 key findings →
Participants: 818 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Most studies investigating the genetics of dementia have focused on Alzheimer disease, but little is known about the genetics of vascular dementia. 4 key findings →
Design: cohort study Participants: 67 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Identifying clinical measures that track disease in the earliest stages of frontotemporal lobar degeneration (FTLD) is important for clinical trials. 4 key findings →
Participants: 31 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Hexanucleotide repeat expansion in C9ORF72 is the most common genetic cause of frontotemporal dementia and motor neuron disease. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
TDP-43 (TAR-DNA binding protein) aggregates in neuronal inclusions in motoneuron disease (MND), as well as in frontotemporal lobar degeneration (FTLD) and FTLD associated with MND (FTLD-MND). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
A liability threshold model of disease was used to estimate heritability of EOAD and late-onset Alzheimer disease (AD) using concordance for AD among parent-offspring pairs. 4 key findings →
Participants: 5,370 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
) within the first intron of SCN8A on chromosome 12 (Figure 1), overlapping a significant region in the previous admixture mapping analysis. eHiCA revealed more and stronger interactions between rs4761988 and SLC4A8, SCN8A and FIGNL2 in EU compared to AF genome (Figure 2), consistent with the admixture mapping result. 4 key findings →
Design: meta-analysis Participants: 867 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Social isolation and loneliness were associated with a greater risk for incident dementia among T2DM individuals, with differential explanatory factors. 3 key findings →
Design: longitudinal study Participants: 24,986 Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Population-based evidence directly linking liver diseases to brain disorders is limited, and its genetic and biochemical associations remain unclear. 2 key findings →
Design: cohort study Participants: 59 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Eight thousand five hundred twenty-one articles were screened, and 75 articles were eligible to be included. 2 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
We replicated the CLU-MS4A4E interaction in a large case-control series and observed APOE ε4 and possible dominant effect. 1 key finding →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The genetic variants play a crucial role in the pathogenesis of Alzheimer's disease (AD), while the relationships of specific single nucleotide polymorphisms (SNPs) with AD are still controversial. 5 key findings →
Design: meta-analysis Participants: 35 Evidence: high
Full summary, score breakdown and related studies → Original source Full text may need a subscription
10 of the 3,521 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 →