Levels of KLK6 and KLK10 were significantly increased in AD. 4 key findings →
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.
Compared to controls, all three clinical groups showed a pattern of mainly increased referenced standard uptake values (SUVR) for the amyloid tracer [18F]-AV45 PET, with rank order PTSD > TBI_PTSD > TBI > Control, and same rank order was seen in the deficits of cognitive functions. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
CSF Aß42 levels were lower, whereas t-tau/Aß42 and p-tau/Aß42 ratios were higher in patients with AD compared with those with FTD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Lumbar puncture (LP) is a common way of collecting cerebrospinal fluid (CSF) both in the clinic and in research. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In Alzheimer's disease patients, although amyloid deposition and CSF amyloid changes continued to "cascade", there was no evidence to suggest that amyloid and tau biomarkers predicted each other, although both amyloid deposition and CSF tau progression predicted cognitive decline independently. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Twenty-seven iNPH, 27 AD, and 18 controls were included. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research investigating treatments and interventions for cognitive decline and Alzheimer's disease (AD) suffer due to difficulties in accurately identifying individuals at risk of AD in the pre-symptomatic stages of the disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In diabetic retinopathy, venous oxygen saturation increases and arteriovenous difference decreases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The ensuing upward shift in demographic distribution due to the increase in life expectancy has resulted in a rising prevalence of Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In terms of the retinal neuronal structure, multiple retinal neuronal layers are significantly thinner in Alzheimer's disease dementia, such as the parapapillary retinal nerve fiber layer (RNFL) and macular ganglion cell-inner plexiform layer (GC-IPL). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The AT(N) research framework was introduced in 2018 to define Alzheimer's disease as a biological entity. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Interest in reliable biomarkers of Alzheimer disease, the leading cause of dementia, has been fuelled by challenges in diagnosing the disease and monitoring disease progression as well as the response to therapy. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of dementia, with no means of cure or prevention. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
ANCOVA (age and schooling as covariates) displayed statistically significant results with respect to CSF biomarkers' profiles regardless of the socio-demographic divergencies previously identified by one-way ANOVA. 5 key findings →
Design: post-hoc analysis Evidence: low
Full summary, score breakdown and related studies → Original source
Among cognitively normal individuals, a 5 μg/m3 increase in 7-day and 1-year average PM2.5 was associated with elevated VCAM-1 (7-day: 35.4 (9.7, 61.1) ng/ml; 1-year: 51.8 (6.5, 97.1) ng/ml). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
HIV-associated neurocognitive disorders (HAND) is a term used to describe a variety of neurological impairments observed in HIV-infected individuals. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The pathology of Alzheimer’s disease (AD), the most common cause of dementia, is considered to be mainly driven by two major hallmarks (tau and amyloid beta). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Blood phospho-tau181 may offer a useful biomarker for Alzheimer’s disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The phosphatase and tensin homologue deleted on chromosome 10 (PTEN) negatively regulates intracellular levels of PIP3 and antagonizes the PI3K signaling pathway important for cell survival. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Basal ganglia, cerebral cortex and subcortical white matter were studied for glial fibrillary acidic protein (GFAP) in four cases of hepatic encephalopathy (HE) with Alzheimer II gliosis and five age-matched controls. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Fluid biomarkers improve the diagnostic accuracy in dementia and provide an objective measure potentially useful as a therapeutic response in clinical trials. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In this study, we aimed to compare cerebrospinal fluid (CSF) levels of total tau (t-tau), phosphorylated tau (p-tau(181)) and positron emission tomography with (18)F-fluorodeoxyglucose (FDG-PET) in the differential diagnosis of Alzheimer's disease (AD) under clinical conditions. 4 key findings →
Design: cross-sectional Participants: 24 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The analyses of the community‐based U.S. POINTER indicate that AA/B individuals present differences in AD and related dementia biomarker values. nHW had higher fully adjusted cognitive scores. 5 key findings →
Participants: 644 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We found ADI*pTau217 interactions on immediate and delayed word recall. 5 key findings →
Participants: 136 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
From across this tag
10 of the 3,322 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.
- Cerebrospinal fluid Aβ and tau level fluctuation in an older clinical cohort
- Neurogranin and Neuronal Pentraxin Receptor as Synaptic Dysfunction Biomarkers in Alzheimer's Disease
- The Role of GFAP as a Marker of Astrocyte Activation in the Pathogenesis of Alzheimer's Dementia: A Literature Review
- Plasma Phosphorylated Tau 217 in Participants at Risk for Chronic Traumatic Encephalopathy
- Correlation Between Brain Structure Atrophy and Plasma Amyloid-β and Phosphorylated Tau in Patients With Alzheimer's Disease and Amnestic Mild Cognitive Impairment Explored by Surface-Based Morphometry
- TDP-43 proteinopathy: the complex biological and clinical findings in LATE-NC, LANS, and other mixed age-related major neurocognitive disorders
- Increased tau in the cerebrospinal fluid of patients with frontotemporal dementia and Alzheimer's disease
- Comparison of CSF phosphorylated tau 181 and 217 for cognitive decline
- Plasma neurofilament light as a potential biomarker of neurodegeneration in Alzheimer's disease
- Additional use of Aβ₄₂/Aβ₄₀ ratio with cerebrospinal fluid biomarkers P-tau and Aβ₄₂ increases the level of evidence of Alzheimer's disease pathophysiological process in routine practice
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 →