28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
In 14 of the 15 suspected HAb cases, HBT treatment greatly reduced measured p-tau217 concentrations. and in one of three specimens selected for further investigation, reduced Aβ42 concentrations PEG precipitation in the three selected samples also reduced p-tau217 concentrations, while serial dilution yielded mixed effects. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Gantenerumab reduced amyloid PET load, CSF biomarkers of amyloid beta (Aβ)40, total tau (t-tau), phosphorylated tau 181 (p-tau181), neurogranin, S100 calcium-binding protein B (S100B), neurofilament light (NfL), alpha-synuclein (α-syn), neuronal pentraxin-2 (NPTX2), and plasma biomarkers of t-tau, p-tau181, p-tau217, and glial fibrillary acidic protein (GFAP) while increasing plasma Aβ40, Aβ42. vMRI showed increased reduction in whole brain volume and increased ventricular expansion, while hippocampal volume was unaffected. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Models including plasma biomarkers yielded the most accurate predictions of tau-PET burden (best model: R-squared = 0.66-0.69), with especially high contribution from plasma phosphorylated tau-217 (p-tau217). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Phosphorylation renders the PRD significantly resistant to cleavage by the lysosome, especially at less acidic pH setpoints. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's Disease (AD) biomarker measurement is key to aid in the diagnosis and prognosis of the disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
An accurate diagnosis of neurodegenerative disease and traumatic brain injury is important for prognostication and treatment. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Elevated BMI/BV associated with lower BBM concentrations, especially for p-Tau217 and NfL, independent of brain amyloid burden. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Participants with SSD exhibited a greater increase in plasma NfL levels and more pronounced declines in global cognition, memory, executive function, language, and processing speed over 2 years compared to non-SSD participants. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) primarily affects older adults. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
As the most prevalent form of dementia, Alzheimer's disease (AD) represents a major public health challenge. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Brain amyloid-β (Aβ) deposition is a hallmark to define Alzheimer's disease (AD). 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma biomarkers were associated with comorbidities and metabolites such as estimated glomerular filtration rate, homocysteine, and high-density lipoprotein. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma+/PET- demonstrated increased FW (24 regions) and decreased FAt (66 regions) compared to plasma-/PET-. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
To investigate amyloid-β (Aβ) in frontotemporal dementia (FTD), cerebrospinal fluid (CSF) Aβ38, Aβ40, and Aβ42 in frontotemporal lobar degeneration (FTLD; N = 18 genetically and/or pathologically confirmed and N = 8 FTD with concomitant amyotrophic lateral sclerosis) were compared with Alzheimer's disease (AD; pathological or Pittsburgh-compound-B Positron-emission-tomography (PIB-PET) positive; N = 25) and controls (N = 24). 3 key findings →
Design: post-hoc analysis Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source
Eighty (22%) participants were APOE ε4 carriers and 290 (73%) were non-carriers. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid β (Aβ) peptides are important components of plaques in patients with Alzheimer's disease (AD). 1 key finding →
Participants: 370 Evidence: low
Full summary, score breakdown and related studies → Original source
Both cohorts revealed diminished choriocapillaris signals, demonstrating the highest discriminatory capability (area under the receiver operating characteristic curve: SS-OCTA 0.913, SD-OCTA 0.991; P < 0.001). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
As the population ages, neurodegenerative diseases are becoming more prevalent, making it crucial to comprehend the underlying disease mechanisms and identify biomarkers to allow for early diagnosis and effective screening for clinical trials. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The life expectancy of people with multiple sclerosis (MS) has increased, yet we have noted that development of a typical Alzheimer disease dementia syndrome is uncommon. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The maximum mean wait time under the current workflow was projected at 6.4 months, decreasing with BBM integration. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
As expected, males had higher lean mass and VO2peak than females (p = 0.01), but groups did not differ in body mass index (p = 0.51). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Specific biomarkers in a readily accessible biological fluid, such as blood, could aid in the identification, characterization, validation, and routine monitoring of Alzheimer's disease (AD) progression. 5 key findings →
Participants: 135 Evidence: low
Full summary, score breakdown and related studies → Original source
GFAP did not correlate with Aβ- or tau-PET cross-sectionally. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Synaptic degeneration is a major hallmark of Alzheimer's disease (AD) and the best pathological correlate of cognitive dysfunction. 3 key findings →
Participants: 64 Evidence: low
Full summary, score breakdown and related studies → Original source
Participants rated the materials highly regarding value and comprehension. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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 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.
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 →