28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Previous studies of Aβ plasma as a biomarker for Alzheimer's disease (AD) obtained conflicting results. 5 key findings →
Design: longitudinal study Participants: 715 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease comorbid pathologic characteristics are common and are associated with more rapid cognitive decline in patients with dementia with Lewy bodies (DLB); therefore, it is anticipated that plasma p-tau concentrations may have utility in assessing cognitive impairment in individuals with this disorder. 4 key findings →
Design: cohort study Participants: 371 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Plasma phosphorylated tau at threonine 181 (p-tau181), a well-validated marker of Alzheimer disease (AD) pathologic change, could be a more efficient way to diagnose AD than invasive or expensive biomarkers requiring CSF or PET. 4 key findings →
Design: cross-sectional Participants: 571 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The ε4 allele of apolipoprotein E (APOE) gene and increasing age are two of the most important known risk factors for developing Alzheimer disease (AD). 4 key findings →
Design: cohort study Participants: 1,593 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
One hundred eighty-seven participants with brain autopsy (NPDx1: AD n = 85; other n = 102; mean age: 74.3 years, 38.5% female; interval blood collection-death [mean ± SD]: 2.8 ± 1.6 years) and 67 NC without brain autopsy (mean age: 66.5 years, 71.6% female) were included. pTau217, but not GFAP, levels increased stepwise with increasing Thal phases (β = 0.61; 95% CI [0.24-0.97] to β = 0.91 [0.55-1.27]) and Braak stages (β = 0.59; [0.16-1.01] to β = 0.74 [0.33-1.15]). 5 key findings →
Design: cohort study Participants: 85 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Despite remarkable progress in the biomarker field in recent years, local validation of plasma biomarkers of Alzheimer’s disease (AD) and dementia is still lacking in Latin America. 5 key findings →
Design: cohort study Participants: 49 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The causes of late onset Alzheimer disease (LOAD) are not known but several recent lines of evidence implicate the adaptive immune system. 3 key findings →
Design: longitudinal study Participants: 72 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma phosphorylated-tau181 (p-tau181) showed the potential for Alzheimer's diagnosis and prognosis, but its role in detecting cerebral pathologies is unclear. 3 key findings →
Design: cross-sectional Participants: 1,189 Evidence: low
Full summary, score breakdown and related studies → Original source
We developed and validated a novel ECL based sandwich immunoassay for the NfL protein in serum (NfL(Umea47:3)); levels in ALS were more than 20-fold higher than in controls. 2 key findings →
Design: longitudinal study Participants: 20 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Serum NFL is increased in ALS in comparison to other conditions and can serve as diagnostic and prognostic biomarker. 2 key findings →
Design: longitudinal study Participants: 124 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The core Alzheimer's disease (AD) cerebrospinal fluid (CSF) biomarkers; amyloid-β (Aß), total tau (t-tau), and phosphorylated tau (p-tau181), are strong indicators of the presence of AD pathology, but do not correlate well with disease progression, and can be difficult to implement in longitudinal studies where repeat biofluid sampling is required. 3 key findings →
Design: longitudinal study Participants: 54 Evidence: moderate
Full summary, score breakdown and related studies → Original source
High levels of Aβ42 and tau in both young controls and DS suggest these proteins are produced by normal physiological processes, whereas the changes seen in later life are consistent with emergence of pathological alterations. 4 key findings →
Design: longitudinal study Participants: 100 Evidence: moderate
Full summary, score breakdown and related studies → Original source
These results strengthen the clinical evidence that AD is accompanied by an inflammatory response, particularly higher peripheral concentrations of IL-6, TNF-α, IL-1β, TGF-β, IL-12 and IL-18 and higher CSF concentrations of TGF-β. 5 key findings →
Participants: 680 Evidence: low
Full summary, score breakdown and related studies → Original source
Data from deformation-based magnetic resonance imaging morphometry demonstrated a Parkinson's disease-specific brain network had more atrophy in the diffuse malignant subtype, with the mild motor-predominant subtype having the least atrophy. 4 key findings →
Design: longitudinal study Participants: 223 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The enrolled population of 84 subjects (31 homozygotes and 53 heterozygotes) was 52% females, mean age 69 years, MMSE 25.7 [70% mild cognitive impairment (MCI), 30% mild AD] with 55% on cholinesterase inhibitors. 5 key findings →
Design: clinical trial Participants: 80 Evidence: low
Full summary, score breakdown and related studies → Original source
Age was the strongest risk factor for progression. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The current results do not support the notion that lithium treatment may lead to reduced hyperphosphorylation of tau protein after a short 10-week treatment in the Alzheimer's disease target population. 2 key findings →
Participants: 38 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma p-tau biomarkers had a greater diagnostic performance and larger effect sizes compared to t-tau and Aβ42/40 assays in detecting Aβ pathology. 5 key findings →
Design: cross-sectional Participants: 197 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We analysed 461 participants from the DABNI and SPIN cohorts. 5 key findings →
Design: cross-sectional Participants: 461 Evidence: low
Full summary, score breakdown and related studies → Original source
We found that plasma p-tau217 was more associated with cognitive performance than p-tau181 and p-tau231 and that this relationship was particularly strong for memory scores (TRIAD: βp-tau217 = -0.53, βp-tau181 = -0.35 and βp-tau231 = -0.24; BioFINDER-2: βp-tau217 = -0.52, βp-tau181 = -0.24 and βp-tau231 = -0.29). 4 key findings →
Design: cross-sectional Participants: 103 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Personality traits have been associated with the risk of dementia and Alzheimer's disease neuropathology, including amyloid and tau. 3 key findings →
Design: longitudinal study Participants: 786 Evidence: moderate
Full summary, score breakdown and related studies → Original source
(N = 558, mean age = 69.2 ± 8.8, 56.5% women) were diagnosed with AD (n = 274, considering dementia and MCI stages), frontotemporal dementia (FTD, n = 55), Lewy body disease (LBD, n = 40, considering MCI and dementia stages), other neurodegenerative diseases, n = 57 (e.g Supranuclear Palsy, Corticobasal syndrome), non-neurodegenerative cognitive impairment (NND, n = 79, e.g. vascular lesions, epilepsy or psychiatric disorders) or subjective cognitive impairment (SCI, n = 53). 4 key findings →
Design: cross-sectional Participants: 558 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We analyzed 128 participants (women: 59%, mean age: 74 years). 5 key findings →
Design: cohort study Participants: 128 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Repetitive Head Impacts (RHI) in boxing may increase the risk for neuronal damage. 3 key findings →
Design: longitudinal study Participants: 15 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Deamidation products of blood albumin were significantly elevated in vascular dementia and frontotemporal dementia (P < 0.05), but less so in PD. 5 key findings →
Design: longitudinal study Participants: 140 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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.
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 →