Individuals with AD had high CSF pT217/T217 and low Aβ42/40. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Individuals with AD had high CSF pT217/T217 and low Aβ42/40. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid β 42/40 concentration quotient has been empirically shown to improve accuracy of the neurochemical diagnostics of Alzheimer's Disease (AD) compared to the Aβ42 concentration alone, but this improvement in diagnostic performance has not been backed up by a theoretical argumentation so far. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The expression of ABCA1 was significantly downregulated in AD models at both mRNA and protein levels. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Based on the reduction of amyloid β plaques, US FDA has recently approved Aducanumab as a disease modifying treatment for Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Reliable quantitative blood biomarkers are important in vascular dementia (VaD) because early diagnosis and therapeutic intervention are effective in preventing progression of dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A timely diagnosis of frontotemporal degeneration (FTD) is frequently challenging due to the heterogeneous symptomatology and poor phenotype-pathological correlation. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Do MRI-based metrics of a CSF-dynamics disorder, disproportionately enlarged subarachnoid-space hydrocephalus (DESH), correlate with discordant amyloid biomarkers (low CSF β-amyloid 1-42, normal Aβ-PET scan)? 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Systemic comorbidity precipitates the risk for dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The One Card Learning Test (OCL80) from the Cogstate Brief Battery-a digital cognitive test used both in-person and remotely in clinical trials and in healthcare contexts to inform health decisions-has shown high sensitivity to changes in memory in early Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The data show that dementia research is exponentially developing following the evolution of widespread use of computer science. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Herein, combined with a pervasive smartphone installed with a color recognition app, dual-responsive CDs@Eu/GMP ICPs were designed as a red-to-blue paper-based colorimetric sensor for the point-of-use analysis of cerebral acetylcholinesterase (AChE) upon Cd2+ exposure. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuroinflammation is a common feature in neurodegenerative diseases, modulated by the Alzheimer's disease risk factor, apolipoprotein E (APOE). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Since the identification of the apolipoprotein E (apoE) *ε4 allele as a major genetic risk factor for late-onset Alzheimer's disease, significant efforts have been aimed at elucidating how apoE4 expression confers greater brain amyloid-β (Aβ) burden, earlier disease onset and worse clinical outcomes compared to apoE2 and apoE3. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Age-related macular degeneration (AMD) is a multifactorial retinal disorder that is a major global cause of severe visual impairment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Though apolipoprotein E ε4 (APOE ε4) is a major genetic risk factor for late-onset Alzheimer's disease, its association with depression remains controversial. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Here, we report that the acute exposure of primary cortical neurons or synaptoneurosomes to APOE4 leads to a significant decrease in global protein synthesis. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
An arginine-rich apolipoprotein was discovered 50 years ago and became known as apolipoprotein E (ApoE) 10 years later. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The ε4 allele of APOE-encoding apolipoprotein (ApoE) is one of the strongest genetic risk factors for Alzheimer's disease (AD). 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, currently affecting 35 million people worldwide. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The genetic locus containing the WWOX and MAF genes was implicated as a clinical Alzheimer's disease (AD) risk locus in two recent large meta-analytic genome wide association studies (GWAS). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's Disease (AD) is the most prevalent form of dementia across the world. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The high prevalence of Alzheimer's disease (AD) among the elderly population and its lack of effective treatments make this disease a critical threat to human health. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Novel therapeutic strategies for Alzheimer's disease (AD) are of the greatest priority given the consistent failure of recent clinical trials focused on Aβ or pTau. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
A multi-stage variable selection method is introduced for detecting association signals in structured brain-wide and genome-wide association studies (brain-GWAS). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disease associated with a complex genetic etiology. 3 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 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 →