28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Synaptic neurodegeneration is thought to be an early event initiated by soluble β-amyloid (Aβ) aggregates that closely correlates with cognitive decline in Alzheimer disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Brain PET adds value in diagnosing neurodegenerative disorders, especially frontotemporal dementia (FTD) due to its syndromic presentation that overlaps with a variety of other neurodegenerative and psychiatric disorders. 18F-FDG-PET has improved sensitivity and specificity compared with structural MR imaging, with optimal diagnostic results achieved when both techniques are utilized. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Successful back-translating clinical biomarkers and molecular imaging methods of Alzheimer's disease (AD), including positron emission tomography (PET), are very valuable for the evaluation of new therapeutic strategies and increase the quality of preclinical studies. 18 F-Fluorodeoxyglucose (FDG)-PET and 18 F-Florbetaben-PET are clinically established biomarkers capturing two key pathological features of AD. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In the 2-month-old mice, sonobiopsy significantly increased the normalized levels of plasma p-tau species compared with the conventional blood-based liquid biopsy (p-tau-181-to-mouse tau [m-tau] ratio: 1.7-fold increase, P = .006; p-tau-231-to-m-tau ratio: 1.4-fold increase, P = .048). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The extracellular deposition of β-amyloid (Aβ) is one of the major characteristics in Alzheimer´s disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Treatment strategies that are efficient against established Alzheimer's disease (AD) are needed. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease (AD) diagnosis is confirmed using a medley of modalities, such as the detection of amyloid-β (Aβ) neuritic plaques and neurofibrillary tangles with positron electron tomography (PET) or the appraisal of irregularities in cognitive function with examinations. 3 key findings →
Participants: 53 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer disease plasma biomarkers have emerged as minimally invasive, cost-effective tools for early diagnosis and disease monitoring yet their stability under common "real world" pre-analytical conditions remains incompletely characterized. 3 key findings →
Participants: 12 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Vascular burden influences NfL levels, particularly in amyloid‐negative individuals. 5 key findings →
Participants: 371 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
We have successfully generated specific high affinity monoclonal antibodies against p -Tau217, p -Tau205, and N-terminus GFAP and have confirmed that these antibodies have the necessary specificity and sensitivity for the Simoa platform. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A total of 143 patients with cognitive concerns were included who underwent a PrecivityAD2 test as part of their clinical evaluation. 5 key findings →
Participants: 4,000 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In the present study, a novel mutation in the presenilin 1 gene was discovered in an Iraq-native patient with early-onset Alzheimer's disease, who presented with speech impairment and memory decline at age 46 years. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The number of patients with Alzheimer's Disease (AD) and other types of dementia disorders has drastically increased over the last decades. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
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 →