27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
The annual number of health insurance claims for p-tau181 testing gradually increased from 1358 (2014) to 3420 (2023); 79-86% of claims were from inpatient settings throughout the study period. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
With the global population rapidly aging, dementia has emerged as a major public health concern. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The advent of disease-modifying treatments and risk-reduction strategies in the clinic have increased the demand for biomarkers for early disease detection, prediction of clinical course of disease, individual risk prediction and monitoring of treatment effects. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The 2nd SAMS score were higher than the 1st SAMS score in some participants, on the other hand, the intraclass correlation coefficient was good. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In this study, we developed a newly designed μPAD for CL immunoassays, leveraging smartphone-based image capture, valve-regulated reaction process, and app-driven result analysis to enable fully automated detection. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Monitoring and assessing the progression of symptoms in neurodegenerative diseases, including Alzheimer's and Parkinson's disease, are critical for improving patient outcomes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E (APOE) is the major lipid transport protein in the brain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The apolipoprotein E (APOE) gene is the strongest genetic risk modifier for Alzheimer's disease (AD), with the APOE4 allele increasing risk and APOE2 decreasing it compared with the common APOE3 allele. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Previous studies in humans and humanized APOE mice have demonstrated APOE-genotype-specific differences in the GMB. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In the SAA-APP knock-in model of dense-cored Aβ deposits resulting from accumulation of protofibrillar-favoring Aβ42, we observed that crossing in human APOE reduced amyloid burden. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
ATP Seahorse assay revealed a reduced mitochondrial and glycolytic ATP production in APOE4 iAstrocytes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The brain is the most cholesterol-rich organ in the body, and ApoE is the main lipid carrier protein in the brain. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD), the most common kind of dementia worldwide, is characterized by elevated levels of the amyloid-β (Aβ) peptide and hyperphosphorylated tau protein in the neurons. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a predominant form of dementia in elderly. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Based on the folding energy (ΔΔG) calculations, mutations G165W and L155W were particularly destabilizing in APOE4. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein E (ApoE) variants are central to Alzheimer's disease (AD), Lewy body dementia (LBD) and Niemann-Pick disease type C (NPC). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The ApoE-ε4 gene is a well-established genetic risk factor for neurodegenerative diseases, such as Alzheimer's disease and multiple sclerosis, which are characterized by axonal demyelination in the central nervous system. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
While preclinical studies suggest that Phosphodiesterase 5 (PDE5) inhibition may reduce cognitive impairment, findings from observational studies on whether PDE5 inhibitors reduce Alzheimer's disease (AD) risk have been inconsistent. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer disease (AD) is a complex and progressive neurodegenerative disorder that accounts for the majority of individuals with dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disorder with profound global impact. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Variants in the triggering receptor expressed on myeloid cells 2 (TREM2) gene have been demonstrated to increase the risk of late-onset Alzheimer's disease (AD) and Nasu-Hakola disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Triggering receptor expressed on myeloid cells 2 (TREM2) is an innate immune receptor abundantly expressed in microglia in the brain. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases, including Alzheimer's and Parkinson's disease, affect an increasing number of people in aging societies, dramatically reducing the quality of life of those affected. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer disease (AD) is a chronic, multifactorial neurodegenerative disease affecting a large proportion of the elderly population with detrimental psychological and socioeconomic impacts. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Growing genetic and pathological evidence has identified microglial dysfunction as a key contributor to the pathogenesis and progression of various neurological disorders, positioning microglia replacement as a promising therapeutic strategy. 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 27,380 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 →