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
Research
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
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
It is not known whether computerized cognitive assessments, like the CogState battery, are sensitive to preclinical cognitive changes or pathology in people at risk for Alzheimer's disease(AD). 4 key findings →
Participants: 71 Evidence: low
Full summary, score breakdown and related studies → Original source
Our main findings support that the UPS pathway may be impaired in AD, and UCH-L1 may serve as an additional CSF biomarker for AD. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
The aim of the present study was to investigate, in patients with Alzheimer's disease (AD), and vascular dementia (VAD), patterns of local release of vascular endothelial growth factor (VEGF) and transforming growth factor-beta (TGF-beta), two cytokines having a pivotal role in hypoxia-induced angiogenesis. 3 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source
This influential 2018 paper proposed defining Alzheimer's disease by what is happening biologically in the brain (amyloid plaques, tau tangles, and neuron loss, measured by scans or spinal fluid tests) instead of by memory symptoms alone. 4 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source
42/100
Non-neurological surgery has both acute and long-term effects on the brain. 3 key findings →
Participants: 35 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Human stem cell models have the potential to provide platforms for phenotypic screens to identify candidate treatments and cellular pathways involved in the pathogenesis of neurodegenerative disorders. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Glial fibrillary acidic protein (GFAP) is the structural protein of the astroglial intermediate filament that forms the morphological basis of astrogliosis. 2 key findings →
Participants: 39 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
We conclude that an inverse correlation between levels of inflammation in cortical areas and plasma NfL levels indicates that microglial activation may initially be protective to axons in AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
This article gives an updated account of the clinical application of cerebrospinal fluid (CSF) biomarkers for Alzheimer disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The AD subjects showed positive correlations between CSF-T-tau and CSF-P-tau versus CSF-Mn (r(s) = 0.22, p = 0.004; r(s) = 0.18, p = 0.021). 4 key findings →
Participants: 264 Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Mild cognitive impairment (MCI) is regarded as the prodromal stage of dementia disorders, such as Alzheimer's disease (AD). 4 key findings →
Participants: 73 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Following the development of the first methods to measure the core Alzheimer's disease (AD) cerebrospinal fluid (CSF) biomarkers total-tau (T-tau), phosphorylated tau (P-tau) and the 42 amino acid form of amyloid-β (Aβ42), there has been an enormous expansion of this scientific research area. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The diagnosis of Alzheimer's disease can be improved by the use of biological measures. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
To study the potential diagnostic value of abnormally phosphorylated tau protein in Creutzfeldt-Jakob disease (CJD) compared to Alzheimer's disease (AD), we determined levels of tau phosphorylated at threonine 231 (p-tau231) and of total tau (t-tau) in cerebrospinal fluid (CSF) of CJD patients, AD patients, and healthy controls (HC). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Between 1992 and 2000, 8 women developed dementia (4 AD, 3 vascular dementia, 1 mixed vascular dementia and AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A number of emerging biomarkers are able to measure synapse injury and loss in the brain and may correlate with cognitive function in AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
The aggregation of fibrils of hyperphosphorylated and C-terminally truncated microtubule-associated tau protein characterizes 80% of all dementia disorders, the most common neurodegenerative disorders. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Breakthroughs in the development of highly accurate fluid and neuroimaging biomarkers have catalysed the conceptual transformation of Alzheimer disease (AD) from the traditional clinical symptom-based definition to a clinical-biological construct along a temporal continuum. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
40/100
Further studies will refine this model and enable the use of biomarkers studied in ADNI clinically and in disease-modifying therapeutic trials. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Treatment of Alzheimer's disease (AD) is significantly hampered by the lack of easily accessible biomarkers that can detect disease presence and predict disease risk reliably. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent findings Plasma biomarkers have significantly improved our understanding of ADRD time-course, risk factors, diagnosis and prognosis. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The neurofilament is the major cytoskeletal structure of myelinated axons. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrospinal fluid (CSF) biomarkers T-Tau and Aβ(42) are linked with Alzheimer's disease (AD), yet little is known about the relationship between CSF biomarkers and structural brain alteration in healthy adults. 3 key findings →
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 28,580 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.
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 28,580 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 →