28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease (AD) is characterized by the formation of extracellular amyloid plaques containing the amyloid β-protein (Aβ) within the parenchyma of the brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cleavage of the amyloid precursor protein's (APP) transmembrane domain (TMD) by γ-secretase is a crucial step in the aetiology of Alzheimer's Disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Previous studies on blood-based biomarkers for Alzheimer's disease suggest a less invasive blood test might be a valuable screening tool for Alzheimer-specific pathology. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Innovations in cryogenic electron microscopy (Cryo-EM) have led to high-quality structures of important proteins such as the ribosome and γ-secretase, the membrane protease that produces Aβ involved in Alzheimer's disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Anomalous neuronal accumulation of Aβ peptides was shown to affect synaptic transmission and contribute to neurodegeneration in Alzheimer's disease (AD) brain. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Familial mutations in C99 can increase the total level of the soluble Aβ peptides produced by proteolysis, as well as the Aβ42/Aβ40 ratio, both of which are linked to the progression of Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Ever since the discovery of APOEɛ4 around 25 years ago, researchers have been excited about the potential of a blood test for Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
To elucidate an involvement of amyloid dysmetabolism in the pathophysiology of depression, we investigated associations of plasma amyloid-β (Aβ) levels with Alzheimer's disease-related changes in neuroimaging and cognitive dysfunction in patients with late-life depression. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD)-a complex disease showing multiple pathomechanistic alterations-is triggered by nonlinear dynamic interactions of genetic/epigenetic and environmental risk factors, which, ultimately, converge into a biologically heterogeneous disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid-β (Aβ) is a key protein in Alzheimer's disease (AD) in that its accumulation induces complex pathological changes. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD), characterized by progressive cognitive decline, is the most prevalent neurodegenerative disease in the elderly. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A plethora of dynamic pathophysiological mechanisms underpins highly heterogeneous phenotypes in the field of dementia, particularly in Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The plasma level of sAPPβ was significantly increased in AD patients than in cognitively healthy controls. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurodegenerative disease without a cure. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The expression of microRNA (miRNA) is influenced by ongoing biological processes, including aging, and has begun to play a role in the measurement of neurodegenerative processes in central nervous system. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A European working group has provided a new set of recommendations for the use of cerebrospinal fluid (CSF) biomarkers in the diagnostic evaluation of Alzheimer disease and mild cognitive impairment. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
CSF Aβ42, total tau (t-tau) and phosphorylated tau (p-tau) significantly differed across the three groups. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In recent years, the idea that sleep is critical for cognitive processing has gained strength. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Identification of neurodegeneration-monitoring biomarkers would be of great clinical value for Alzheimer's disease (AD) diagnosis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
With increasing prevalence of Alzheimer's disease (AD) and advances in research of therapeutic approaches, an early and accurate in-vivo diagnosis is crucial. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Specific changes in personality profiles may represent early non-cognitive symptoms of Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a neurodegenerative disease affecting the brain. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Levels of KLK6 and KLK10 were significantly increased in AD. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We found that race modifies the relationship between functional connectivity of default mode network subsystems and cognitive performance, tau, and amyloid levels. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Compared to controls, all three clinical groups showed a pattern of mainly increased referenced standard uptake values (SUVR) for the amyloid tracer [18F]-AV45 PET, with rank order PTSD > TBI_PTSD > TBI > Control, and same rank order was seen in the deficits of cognitive functions. 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 →