27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
In this cross-sectional study (n=272), plasma pTau217/Aβ42 ratio test accuracy was 90% in Veterans without TBI history, but was significantly lower (63-78% accuracy) in Veterans with TBI history, with lowest accuracy in those with greater TBI severity. 5 key findings →
Design: cohort study Participants: 93 Evidence: moderate
Full summary, score breakdown and related studies → Original source
An age-related decline in vasodilation mediated by neurovascular nitric oxide (NO) and vasoconstriction driven by the Piezo1 receptor precede the aggregation of soluble brain proteins such as amyloid-β (Aβ), which then causes further disruption of brain solute homeostasis, ultimately leading to neurodegeneration in Alzheimer’s disease. 1 key finding →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source
Untargeted mass spectrometry remains underutilised for blood-based biomarker discovery in dementia research from large cohorts, where affinity-based approaches dominate. 3 key findings →
Participants: 14,258 Evidence: low
Full summary, score breakdown and related studies → Original source
The analytic sample included 4,465 individuals (mean age 69.7±10.4 years; 58.7% female; 75.8% non-Hispanic White). 4 key findings →
Design: longitudinal study Participants: 51 Evidence: moderate
Full summary, score breakdown and related studies → Original source
a Structured abstract BACKGROUND Over the past couple of decades, the role of infections, as well as the involvement of the immune system, have been highlighted in the development of dementia. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Compared to the CN group, both MCI (β=−1.25, SE=0.19, p <.001) and AD dementia (β=−1.52, SE=0.16, p <.001) participants had lower Brain & Vascular Health composite scores. 3 key findings →
Participants: 197 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The clock claims are unsupported. 3 key findings →
Design: longitudinal study Participants: 83 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease primarily affecting motor neurons but also frequently involving cognitive impairment. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer’s disease is diagnosed after a decade-long phase in which pathology accumulates; current markers show that pathology is present, but not how far it has advanced. 5 key findings →
Participants: 609 Evidence: low
Full summary, score breakdown and related studies → Original source
Chitinase-3-like protein 1 (CHI3L1) is elevated in Alzheimers disease (AD), but its role in glial dysfunction and therapeutic tractability remain unclear. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
CSF DDC reflects nigrostriatal dopaminergic dysfunction, representing a potential quantitative biochemical alternative to DaT-SPECT that might be readily implemented via automated immunoassays. 2 key findings →
Participants: 891 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) flow and the glymphatic system are essential for maintaining brain homeostasis, yet the precise mechanisms driving their profound failure in Alzheimer’s disease (AD) remain largely elusive. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Frontotemporal lobar degeneration (FTLD), predominantly comprised of tau and TDP-43 proteinopathies, is a common cause of early-onset dementia. 3 key findings →
Participants: 566 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) contains brain derived proteins that can be leveraged as biomarkers for Alzheimer’s disease (AD) and other neurodegenerative diseases. 5 key findings →
Participants: 48 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Apolipoprotein E (APOE) genotype is theorised to influence dementia risk partly through effects on blood–brain barrier (BBB) function, but clinical studies examining APOE effects on BBB biomarkers report inconsistent results. 5 key findings →
Design: systematic review Participants: 5,375 Evidence: high
Full summary, score breakdown and related studies → Original source
The global burden of dementia is heavily concentrated in low- and middle-income countries (LMICs), yet biological diagnosis of Alzheimer’s Disease (AD) relies on positron emission tomography (PET) and cerebrospinal fluid (CSF) analysis that are operationally inaccessible in these regions. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid β (Aβ) plaques are a hallmark of Alzheimer’s disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The choroid plexus (CP) maintains brain homeostasis through cerebrospinal fluid production and formation of the blood-cerebrospinal fluid barrier, and its dysfunction has been linked with aging and neurological disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genetic variation in APOE , which encodes a lipid transporter apolipoprotein E (apoE), is the strongest risk factor for late-onset Alzheimer’s disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid-beta (Aβ) accumulation in the brain is linked to Alzheimer’s disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) flows through perivascular spaces (PVSs) surrounding brain vasculature, and impaired flow has been linked to neurodegenerative diseases such as Alzheimer’s. However, the mechanisms driving CSF flow and its oscillatory dynamics remain poorly understood. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Physiological pulsations maintaining brain neurofluidic homeostasis are altered early in the course of Alzheimer’s disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Sixty participants (30 intervention, 30 control) were recruited and followed up between March 2024 to September 2025. 5 key findings →
Design: randomized controlled trial Evidence: high
Full summary, score breakdown and related studies → Original source
Four main themes were extracted: (1) Positive experiences, including perceived improvement in cognitive function and mood; (2) Facilitators and barriers to training participation, with facilitators comprising dementia care experience, higher educational attainment, and availability of free time, and barriers including unfamiliarity with computer operation, low awareness of cognitive training, and lengthy training sessions; (3) Training content preferences, reflecting a desire for both relaxed, engaging content and professional guidance; and (4) Practical dilemmas and suggestions, including difficulties in understanding task instructions and complex login procedures, with recommendations for detailed task descriptions and simplified procedures. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although smartphone usage time is not directly associated with ikigai in older adults, it may reflect preserved physical and cognitive abilities required to navigate digital environments. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
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 →