Traumatic brain injury (TBI) is a major cause of morbidity and mortality, both in adult and pediatric populations. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Traumatic brain injury (TBI) is a major cause of morbidity and mortality, both in adult and pediatric populations. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Macrophage recognition of Salmonella enterica serovar Typhimurium leads to a cascade of signaling events, including the activation of Src family and Syk kinases and the production of reactive oxygen species (ROS), which are critical for host innate defense during early stages of bacterial infection. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the most common cause of dementia. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a common and increasing societal problem due to the extending human lifespan. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
A total of 85 patients were included in the study with rare genotypes excluded from analysis (3 patients). 5 key findings →
Participants: 85 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We observed differential cellular effects on β-amyloid, pTau217 and cognitive measures. 3 key findings →
Participants: 734 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Late-life dementia has a strong heritable component. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The first SVD component accounted for 21.56%, 12.93%, 11.91% of the total co-variability between the pairs (cortical thickness, tau), (relative GM density, tau) and (absolute GM density, tau), respectively. 5 key findings →
Design: cross-sectional Participants: 222 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The genetic architecture of sporadic Early-Onset Alzheimer Disease (sEOAD, onset ≤65 years) remains largely unknown. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Familial frontotemporal dementia (fFTD) is an autosomal dominant heritable form of FTD, onsetting in mid-life, characterized by behavioral and personality changes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The developmental origin of Alzheimer disease (AD) has been proposed but is arguably debated. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We estimated the overall concentration (mean standardized values) and principal components (PCs) of the proteomics and lipidomics data independently. 5 key findings →
Participants: 1,372 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
TDP-43 seeding activity was detected in 67% of TDP-43-linked symptomatic patients, with a specificity of 93%. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
While neuropathological and genetic studies have established the crucial involvement of TDP-43 proteinopathy in the pathogenesis of amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) and related neurodegenerative disorders, multiple studies have described the presence of TDP-43 inclusions in muscular disorders, including inclusion body myositis but also other related rimmed vacuole myopathies. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
• EEG microstate analyses were performed in a cohort of autosomal dominant AD. • Coverage of class C decreased in symptomatic mutation carriers • Coverage of class D decreased in presymptomatic and symptomatic mutation carriers. • Coverage of class E increased in presymptomatic and symptomatic mutation carriers. • The findings may support presymptomatic changes in resting-state neuronal networks. 4 key findings →
Participants: 99 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
variants) was not associated with small vessel stroke (odds ratio [OR], 1.02 [95% CI, 0.95-1.10]), magnetic resonance imaging-confirmed lacunar stroke (OR, 0.95, [95% CI, 0.81-1.11]), nonlobar intracerebral hemorrhage (OR, 1.04 [95% CI, 0.72-1.50]), or vascular dementia (OR, 1.09 [95% CI, 0.95-1.25]). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
APOE ε4 is associated with accelerated progression of AD pathology. 3 key findings →
Participants: 575 Evidence: low
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We suggest that the APP23 Tg mouse may develop an earlier blockage in A beta clearance than the Tg2576 mice, resulting in a more severe accumulation of A beta in the perivascular drainage pathways and in the brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Frontotemporal lobar degeneration (FTLD) is a clinically and pathologically heterogeneous syndrome, characterized by progressive decline in behaviour or language associated with degeneration of the frontal and anterior temporal lobes. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Frontotemporal dementia is commonly associated with parkinsonism in several sporadic (i.e., progressive supranuclear palsy, corticobasal degeneration) and familial neurodegenerative disorders (i.e., frontotemporal dementia associated with parkinsonism and MAPT or progranulin mutations in chromosome 17). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The major component of senile plaques found in the brains of Alzheimer disease patients is the beta-amyloid peptide, which is derived from a larger amyloid precursor protein (APP). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Recent human genetic studies have challenged long standing hypotheses about the chain of events in Alzheimer's disease (AD), as the identification of genetic risk factors in microglial genes supports a causative role for microglia in the disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Trem2 is an orphan, DAP12 associated receptor constitutively expressed in vivo by subsets of microglia in the healthy adult murine CNS and in vitro by subsets of oligodendrocytes in neonatal mixed glial cultures. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The triggering receptor expressed on myeloid cells 2 (TREM2) is an immune-modulatory receptor involved in phagocytosis and inflammation. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Recent research has shown that the triggering receptor expressed on myeloid cells 2 (TREM2) in microglia is closely related to the pathogenesis of Alzheimer's disease (AD). 4 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →