Plasma and CSF NFL concentrations were very highly correlated (r = 0.89, P < 0.0001). 1 key finding →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Research
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Cognitive deficits and depression appear to be more common in aging former NFL players compared with healthy controls. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
We constructed a standardized operating procedure for plasma handling, to facilitate introduction of blood-based biomarkers into the research and clinical settings. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Experimental studies indicate that overactivation of the DNA repair protein poly(ADP-ribose) polymerase (PARP) in response to oxidative damage to DNA can cause cell death due to depletion of NAD+. 3 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source
47/100
It is currently unclear how amyloid-β and tau deposition are linked to changes in synaptic function and axonal structure over the course of Alzheimer's disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In this study, we determined the diagnostic accuracy of cerebrospinal fluid (CSF) biomarkers to predict development of Alzheimer's disease (AD) within five years in patients with mild cognitive impairment (MCI). 1 key finding →
Participants: 94 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The combination of decreased amyloid β42 (Aβ42) and increased total tau proteins (T-Tau) and phosphorylated tau (P-Tau) in cerebrospinal fluid (CSF) has recently been considered as a biological diagnostic criterion of Alzheimer's disease (AD). 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
A blood-based biomarker of Alzheimer's disease (AD) progression could be instrumental in targeting asymptomatic individuals for treatment early in the disease process. 3 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
This study strengthens the potential of neurogranin as an AD CSF biomarker, which now needs validation in larger studies. 3 key findings →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source
Our findings support an association between neuroaxonal injury and delirium. 3 key findings →
Participants: 130 Evidence: low
Full summary, score breakdown and related studies → Original source
The study shows that higher serum NFL tertile levels correlate with increased risk of cognitive stage transition in both MCI and CU participants. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Blood-based tests have sparked tremendous attention in non-invasive early diagnosis of Alzheimer's disease (AD), a most prevalent neurodegenerative malady worldwide. 3 key findings →
Participants: 27 Evidence: low
Full summary, score breakdown and related studies → Original source
To determine whether apparent involvement of DYRK1A in Alzheimer's disease (AD) pathology makes it a candidate plasma biomarker for diagnosis, we developed a method to quantify plasma DYRK1A by immunoblot in transgenic mouse models having different gene dosages of Dyrk1a, and, consequently, different relative protein expression. 4 key findings →
Participants: 26 Evidence: low
Full summary, score breakdown and related studies → Original source
The aim of this study was to explore concentrations differences of soluble amyloid precursor protein (sAPP) α and β in blood plasma in patients with probable Alzheimer's disease (AD) and cognitively healthy age-matched control subjects, as well as patients with behavioural variant frontotemporal dementia (bvFTD). 2 key findings →
Participants: 80 Evidence: low
Full summary, score breakdown and related studies → Original source
Higher HOMA-IR was associated with higher sAβPPβ and Aβ42 . 4 key findings →
Participants: 70 Evidence: low
Full summary, score breakdown and related studies → Original source
The predictive value of Aβ42 was highly affected by the type of collection tube used. 5 key findings →
Participants: 1,966 Evidence: low
Full summary, score breakdown and related studies → Original source
Mean +/- SD CSF NFL levels were increased in patients with FTD (1442 +/- 1183 pg/mL; p < 0.05) and LAD (1006 +/- 727 pg/mL; p < 0.001) compared with control subjects (241 +/- 166 pg/mL) and in LAD compared with EAD (498 +/- 236 pg/mL; p < 0.05), and tended to be increased in FTD compared with EAD. 5 key findings →
Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source
46/100
The differential diagnosis of Parkinson's diseases (PD) is challenging, especially in the early stages of the disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Amyloid plaques appear early during Alzheimer's disease (AD), and their development is intimately linked to activated astrocytes and microglia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Florbetapir F 18 selectively binds Aβ in human brain tissue. 4 key findings →
Participants: 40 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The search for accessible and cost-effective biomarkers to complement current cerebrospinal fluid (CSF) and imaging biomarkers in the accurate detection of Alzheimer disease (AD) and other common neurodegenerative disorders remains a challenging task. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
SIs on the LASSI-L related to PSI and frPSI uniquely differentiated Amy+ and Amy- participants with aMCI and likely reflect deficits with inhibition and source memory in preclinical AD not captured by traditional cognitive measures. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In this article, the challenges faced by several noted population studies for Alzheimer dementia in operationalizing current clinical diagnostic criteria for Alzheimer's disease (AD) have been reviewed. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The budgetary impacts are not insignificant but are small in comparison to the likely market price of any disease-modifying treatments or to the probable costs of missed or inaccurate diagnosis. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We investigated whether blood N-glycan changes can be used as a diagnostic biomarker for Alzheimer disease (AD). 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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 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.
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 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 →