Recent advances in biomarkers provide the possibility of early or preclinical diagnosis of Alzheimer's pathology. 5 key findings →
Participants: 25 Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
These findings show that sleep loss alters some plasma AD biomarkers by lowering brain clearance mechanisms and needs to be taken into account when interpreting individual plasma AD biomarkers but not ratios. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These results suggest that the targeted methylation of APP via dCas9-Dnmt3a treatment can be a potential therapeutic strategy for AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Production of amyloid β-protein (Aβ) is carried out by the membrane-embedded γ-secretase complex. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Measurement of Aβ in plasma contributes to addressing the amyloid component of the ATN (amyloid/tau/neurodegeneration) framework and could be a first step before or in place of a PET or cerebrospinal fluid screening study. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These results indicate that an increase in the baseline level of amyloid peptides, which are associated with an increase in p-tau (181), may be a biological characteristic and possibly a risk factor for AD. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's Disease (AD) is a progressive neurodegenerative disease characterized by amyloid-β (Aβ) plaque deposition and neurofibrillary tangle accumulation in the brain. 5 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings support a role for plasma GFAP as a clinical biomarker of Aβ-related astrocyte reactivity that is associated with cognitive decline and neurodegeneration. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma biomarkers could revolutionize many areas of the AD diagnostic pathway and care continuum, but further research is needed. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Consistent with current views, capacity reflected an interaction between the decision-maker and the demands of the decision-making task. 2 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source
Lowered 3alpha,5alpha-THP levels appear promising as a biomarker in dementia, but further work is needed to establish the sensitivity and specificity of these findings in AD. 4 key findings →
Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source
In the 115 years since the discovery of Alzheimer's disease (AD), our knowledge, diagnosis, and therapeutics have significantly improved. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
Better diagnostic tools at initial evaluation may reduce unnecessary delays in access to treatment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Different authors described that transthyretin (TTR) is decreased in the cerebrospinal fluid (CSF) of Alzheimer's disease (AD) patients and thus TTR is a potential CSF biomarker in AD. 4 key findings →
Participants: 55 Evidence: low
Full summary, score breakdown and related studies → Original source
The past few years have seen an explosion in sensitive and specific assays for cerebrospinal fluid (CSF) and blood biomarkers for Alzheimer's disease (AD) and related disorders, as well as some novel assays based on pathological seed-induced protein misfolding in patient samples. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
MDS-OAβ to measure plasma Aβ oligomerization is a valuable blood-based biomarker for clinical diagnosis of AD, with high sensitivity and specificity. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
43/100
We have further demonstrated the association of PPY and IgM with NAB, despite technical differences between studies. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Blood-based tests for the differential diagnosis of Alzheimer's disease (AD) are under intensive investigation and have shown promising results with regard to Abeta40 and Abeta42 peptide species in incipient AD. 2 key findings →
Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source
Our data suggest that AD-related biomarkers are altered by food intake. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Although Alzheimer's disease (AD) is the most common neurodegenerative disease, there are still no drugs available to treat or prevent AD effectively. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Multifactorial mechanisms underlying late-onset Alzheimer's disease (LOAD) are poorly characterized from an integrative perspective. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our understanding of Alzheimer's disease (AD) pathophysiology remains incomplete. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The sleep-wake cycle regulates interstitial fluid (ISF) and cerebrospinal fluid (CSF) levels of β-amyloid (Aβ) that accumulates in Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The recently developed ultrasensitive bio-barcode assay was used to measure the concentration of amyloid-beta-derived diffusible ligands (ADDLs), a potential soluble pathogenic Alzheimer's disease (AD) marker, in the cerebrospinal fluid (CSF) of 30 individuals. 4 key findings →
Participants: 30 Evidence: low
Full summary, score breakdown and related studies → Original source
These results demonstrate increased production of the proinflammatory cytokine, TNFalpha and decreased production of the anti-inflammatory cytokine TGFbeta in patients with MCI at risk to develop AD, suggesting a propensity towards inflammation in this patient group and indicating that CNS inflammation is a early hallmark in the pathogenesis of AD. 3 key findings →
Participants: 56 Evidence: low
Full summary, score breakdown and related studies → Original source
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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.
What this library is — and isn't
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 →