27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The CSF Abeta42/Abeta40 ratio improves differentiation of AD patients from VaD, DLB and non-AD dementia patients, when compared to Abeta42 alone, and is a more easily interpretable alternative to the combination of Abeta42, p-tau and t-tau when differentiating AD from either FTD or non-AD dementia. 4 key findings →
Participants: 69 Evidence: low
Full summary, score breakdown and related studies → Original source
Our results support further efforts to prospectively validate the use of Q Abeta42/p-tau as a biomarker to discriminate between AD and VaD. 2 key findings →
Participants: 86 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma NfL indicates neurodegeneration while plasma p-tau181 levels can serve as a biomarker of cerebral AD pathology and cognitive decline. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The blood-brain barrier (BBB) protects the brain but is also an important obstacle for the effective delivery of therapeutics in Alzheimer's disease and other neurodegenerative disorders. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our results suggest that pericyte injury contributes to AD progression in the early stage in an Aβ-independent pathway. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Increasing life expectancy has led to an aging population, which has consequently increased the prevalence of dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent studies highlight phosphorylated tau (p-tau) at threonine tau 217 (p-tau217) as a new promising plasma biomarker for pathological changes implicated in Alzheimer's disease (AD), but the specific brain pathological events related to the alteration in p-tau217 plasma levels are still largely unknown. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
For many years, blood-based biomarkers for Alzheimer's disease seemed unattainable, but recent results have shown that they could become a reality. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative disorders such as Alzheimer's disease (AD) represent a mounting public health challenge. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Biomarkers of neurodegeneration and neuronal injury have the potential to improve diagnostic accuracy, disease monitoring, prognosis, and measure treatment efficacy. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Multiple variables affect plasma biomarkers of amyloid pathology and neurodegeneration among CU in the general population. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Four fluid-based biomarkers have been developed into diagnostic tests for Alzheimer's disease (AD) pathology: the ratio of 42 to 40 amino acid-long amyloid β, a marker of plaque pathology; total-tau and phosphorylated tau, markers of AD-related changes in tau metabolism and secretion; and neurofilament light, a marker of neurodegeneration. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The PrecivityAD™ assays are precise, accurate, sensitive, and linear over a wide analytical range, free from significant interferences, and suitable for use in the clinical laboratory. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
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
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
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
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
10 of the 2,804 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 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.
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 →