28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
These data indicate that the AD genetic architecture influences cognitive and CSF phenotypes in DS adults, supporting common pathways that influence memory decline in both traits. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Except for Aβ42/40, plasma biomarkers are heritable. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The aggregation of the amyloid-β (Aβ) peptides (Aβ42/Aβ40) into amyloid fibrils and plaques is one of the molecular hallmarks in dementia and Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Offspring with a family history of LOAD on the maternal side have lower Aβ42 and Aβ42/40 ratio in the CSF, and maybe at higher risk for developing AD. 3 key findings →
Participants: 162 Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid β and alpha 1-antichymotrypsin (ACT) play an important role in the pathogenesis of sporadic Alzheimer's disease (AD). 2 key findings →
Participants: 112 Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) core biomarkers of Alzheimer's disease (AD), including amyloid peptide beta-42 (Aβ42), Aβ42/40 ratio, and phosphorylated tau (pTau), are precious tools for supporting AD diagnosis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This study aimed to compare serum amyloid processing biomarkers among HIV subtype B (n = 25), HIV subtype C (n = 26), healthy HIV-negative controls (n = 18), and patients with Alzheimer's disease (AD; n = 24). 5 key findings →
Participants: 25 Evidence: low
Full summary, score breakdown and related studies → Original source
Although additional and more diverse cohorts are needed for further clinical validation of the robustness, the miRNA signature appears to be a promising blood test to diagnose AD. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Gene therapy to treat hereditary disorders conventionally delivers the normal allele to compensate for loss-of-function mutations. 2 key findings →
Evidence: preliminary
Full summary, score breakdown and related studies → Original source Free full text
Medicare Part D drug spending was substantial, increasing with dual-eligibility duration: $8732-$9107 among beneficiaries with full-year dual eligibility and exceeding $11 500 among those with 5+ chronic conditions. 1 key finding →
Design: cross-sectional Participants: 1,372,696 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Burden of chronic intravenous treatments exceed the gross medical and social care cost savings and value of caregiver benefit. 3 key findings →
Design: modelling Evidence: preliminary
Full summary, score breakdown and related studies → Original source Free full text
We previously reported that T96K is a gain-of-function mutation in TREM2 based on its ability to increase ligand-dependent activation. 3 key findings →
Evidence: early
Full summary, score breakdown and related studies → Original source Free full text
We determined whether oxidative stress is an early event in the pathogenesis of sporadic Alzheimer disease (AD), and correlated oxidative stress with neuropsychological functions and neurofibrillary pathology in AD and mild cognitive impairment (MCI). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer disease (AD) is the most prevalent neurodegenerative disorder leading to dementia in the elderly. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Imbalance in production and clearance of amyloid beta (Aβ) is the primary reason for its deposition in Alzheimer disease. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Currently, 3 amyloid PET tracers are approved and commercially available for clinical use. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Establishing a diagnosis of Alzheimer dementia can be challenging, particularly early in the course of the disease. 5 key findings →
Evidence: low
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Glutamate transporter solute carrier family 1, member 2 (GLT1/EAAT2), a major modulator of glutamate homeostasis in astrocytes, is assessed in post-mortem human brain samples of frontal cortex area 8 in advanced stages of Alzheimer disease (AD) and terminal stages of dementia with Lewy bodies (DLB) in order to gain understanding of astrogliopathy in diseases manifested by dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Hyperphosphorylated tau protein deposits and, inflammatory processes are characteristic components of Alzheimer disease (AD) pathology. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Glial fibrillary acidic protein (GFAP) is a well-established astrocytic biomarker for the diagnosis, monitoring and outcome prediction of traumatic brain injury (TBI). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Clinical trials to advance the diagnosis and treatment of Alzheimer disease (AD) may expose research subjects to discrimination risks. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In a population-based sample, increasing gliosis precedes development of Alzheimer lesions. 3 key findings →
Evidence: moderate
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Quantification results using the proposed deep learning-based method showed stronger correlations with the FreeSurfer estimates than SPM-based SN using MRI did. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Recent functional magnetic resonance imaging studies have demonstrated that moment-to-moment variability in the blood oxygen level-dependent (BOLD) signal is related to age differences, cognition, and symptomatic Alzheimer's disease (AD). 1 key finding →
Participants: 321 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Brain 18F-FDG PET scans interpreted with Neurostat and 3D-SSP displays accurately detected Alzheimer disease in patients with primary progressive aphasia or corticobasal syndrome as focal-onset dementias. 2 key findings →
Participants: 94 Evidence: moderate
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. 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 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 →