Hematopoietic stem cells contribute to mammalian brain tissue regeneration by transdifferentiation processes. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Hematopoietic stem cells contribute to mammalian brain tissue regeneration by transdifferentiation processes. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
High-throughput plasma Aβ42/40 LC-MS/MS assays can help identify patients with low likelihood of AD pathology, which can reduce PET evaluations, allowing for cost savings. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings suggest a temporal sequence of events in App NL-F/NL-F knock-in mice, in which initial deposition of Aβ aggregates in the brain is followed by a decline of the Aβ42/Aβ40 ratio in CSF and serum once the cerebral Aβ pathology becomes significant. 4 key findings →
Participants: 48 Evidence: low
Full summary, score breakdown and related studies → Original source
ECM proteins do not reflect AD-pathology in CSF. 2 key findings →
Participants: 50 Evidence: low
Full summary, score breakdown and related studies → Original source
Activation of inflammatory processes has been observed within the brain as well as periphery of subjects with Alzheimer's disease (AD). 3 key findings →
Participants: 153 Evidence: low
Full summary, score breakdown and related studies → Original source
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
These proteins can serve as potential blood markers for the diagnosis of AD and EO can suppress their level. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Future studies should develop integrative models that consider nutrition, metabolism, and inflammation to address and fully exploit biomarker utility as well as support precision medicine approaches. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Type 2 diabetes (T2D) is a significant risk factor for Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) and Alzheimer's disease-related disorders (ADRD) are progressive neurodegenerative diseases without cure. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
This article introduces an alternative immunodiagnostic approach based on the concept of a "tauosome" - the diverse set of tau fragments present within biological fluids. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A relationship between Alzheimer's disease (AD) and folate has been reported. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Blood-based biomarkers (BBMs) for Alzheimer's disease (AD) have advanced rapidly and may be a critical tool for broad community-based screening for AD and detection of AD pathology in individuals with cognitive impairment. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
CRISPR-Cas proteins from bacteria are powerful tools for gene editing and molecular diagnostics. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Serum-NfL could be utilized as an accurate surrogate marker of CSF levels to segregate symptomatic CHMP2B carriers, presymptomatic carriers, and non-carriers. 3 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Current experimental outcomes provide a comparative analysis of various machine learning classifiers and confirm that using ensemble-based methods has improved medical diagnostic tasks. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Global aging populations are facing increased prevalence of mild cognitive impairment (MCI) - the preclinical stage of dementia characterized by single/multi-domain neurocognitive decline that does not impair an individual's normal daily functioning. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The common, late onset form of Alzheimer's disease (AD) selectively impacts higher brain circuits, with tau pathology and neurodegeneration preferentially afflicting glutamatergic neurons in the limbic and association cortices. 1 key finding →
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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →