27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Cerebral small vessel disease (CSVD) is strongly linked to metabolic risk factors and represents a major cause of vascular cognitive impairment and dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau pathology, characterized by the aberrant aggregation and accumulation of tau in neurons and glial cells, plays a critical role in the onset and progression of multiple neurodegenerative diseases. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The observed phenotypic and genetic associations highlight shared underlying mechanisms among plasma biomarkers. 2 key findings →
Participants: 696 Evidence: low
Full summary, score breakdown and related studies → Original source
Identifying scalable, objective markers of dementia risk is essential for early prevention and intervention. 3 key findings →
Participants: 562 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Semi-supervised multimodal fusion improves prediction and reveals interpretable imaging patterns that predict APOE4 and clinical diagnoses better than traditional approaches. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Shorter sleep duration and greater REM sleep variability may index early AD-related brain changes, warranting longitudinal studies to establish their prognostic significance. 2 key findings →
Design: longitudinal study Evidence: high
Full summary, score breakdown and related studies → Original source
Biases in cognitive/functional screening tests may disproportionately exclude ethnoracial minorities in AD prevention trials. 1 key finding →
Participants: 6,669 Evidence: low
Full summary, score breakdown and related studies → Original source
NODDI-derived ODI is associated with tau PET signal, even in preclinical disease and may discriminate individuals with-and without tau beyond the MTL. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These therapies require complex diagnostic workup and safety monitoring, raising significant budget impact concerns for healthcare payers. 2 key findings →
Participants: 11,568 Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative research has long hypothesized that aggregated proteins such as amyloid‑β (Aβ), tau, and α‑synuclein (αSyn) are intrinsically toxic and are directly associated with the etiologies of Alzheimer’s disease (AD) and Parkinson’s disease (PD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The occurrence of amyloid-related imaging abnormalities (ARIA), found in clinical trials for Aβ-immunotherapy, has been related to the antibody’s effector function on glial activation by the Fc portion of the antibody. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our study examined the safety and tolerability of centralized lecanemab administration across a widely distributed region and suggests that use of distributed infusion sites increases access to disease-modifying treatment without significant increase in risk. 2 key findings →
Participants: 70 Evidence: low
Full summary, score breakdown and related studies → Original source
The complete absence of ARIA distinguishes XPro1595 from amyloid-targeting therapies and supports its potential for use in combination strategies and potentially for those at a higher risk of ARIA. 5 key findings →
Design: clinical trial Evidence: high
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by abnormal aggregation of the tau protein. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In Alzheimer’s disease (AD) and related tauopathies, progressive pathology has been linked to prion mechanisms whereby ordered tau assemblies, or “seeds,” form in one cell and transit to neighboring or connected cells where they serve as templates for their own replication. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma pTau-181 demonstrates flat or declining longitudinal trajectories and minimal cognitive correlation, suggesting tau is a static biomarker rather than a dynamic therapeutic target in mid-to-late adulthood. 2 key findings →
Design: cross-sectional Participants: 2,523 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A robust method was developed to produce and optimize GST-Tau as a coating antigen for indirect ELISA. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Current Alzheimer’s disease (AD) immunotherapeutics face efficacy and safety limitations with antibody-based approaches. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tauopathies are neurodegenerative diseases characterized by pathological tau accumulation, leading to motor and neuropsychiatric symptoms. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Among adults with obesity or overweight with a weight related condition, there was no difference in the risk of PD or Parkinsonian disorders between GLP-1 RA users and non-users. 4 key findings →
Design: cohort study Participants: 11,683 Evidence: moderate
Full summary, score breakdown and related studies → Original source
DESI is a robust, fully automated MRI biomarker that sensitively detects CSF redistribution characteristic of DESH in iNPH. 1 key finding →
Design: longitudinal study Participants: 1,032 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In a recent open-label, single-arm study, vortioxetine, an antidepressant, was associated with improved cognitive function in patients with MCI, however, no placebo-controlled studies have been conducted to support these findings. 5 key findings →
Design: randomized controlled trial Evidence: high
Full summary, score breakdown and related studies → Original source
Our findings demonstrate differential effects of nicotine on AD risk and smoking intensity on white matter integrity, requiring triangulation with complementary methodological approaches to better inform potential long-term risks of nicotine intake on neurocognitive outcomes. 3 key findings →
Design: cohort study Participants: 334,757 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The high incidence of new prescribing, as well as the lack of deprescribing, points to unmet needs and a role for more proactive medication review. 3 key findings →
Participants: 3,713 Evidence: low
Full summary, score breakdown and related studies → Original source
Large language models (LLMs) offer new opportunities to synthesize the vast and heterogeneous biomedical literature, yet their potential to support drug target prioritization in complex diseases such as Alzheimer’s disease (AD) remains largely unexplored. 1 key finding →
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →