31,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease (AD), a progressive neurodegenerative disease characterized by impairments of cognitive function as a result of synaptic deficits and neuronal loss, is associated with inflammation. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Intramembrane proteolysis of transmembrane substrates by the presenilin-γ-secretase complex is preceded and regulated by shedding of the substrate's ectodomain by α- or β-secretase. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The complement system plays critical roles in development, homeostasis, and regeneration in the central nervous system (CNS) throughout life; however, complement dysregulation in the CNS can lead to damage and disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Hyperhomocysteinemia is recognized as a risk factor for several diseases, including cardiovascular and neurological conditions. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The overlapping symptoms of behavioural variant frontotemporal dementia (bvFTD) and primary psychiatric disorders (such as depressive disorder, schizophrenia spectrum, and bipolar disorder) present a challenge for the differential diagnosis of bvFTD in middle and older-aged people. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of neurodegenerative dementia and there is no cure to date. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The development of blood-based biomarkers of Alzheimer's disease (AD) pathology as tools for screening the general population, and as the first step in a multistep process to determine which non-demented individuals are at greatest risk of developing AD dementia, is essential. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid-β (Aβ) oligomers largely initiate the cascade underlying the pathology of Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
CSF neurofilament contributes to a panel of CSF α-synuclein species in differentiating PD patients from healthy controls. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The implication of epigenetic mechanisms in Alzheimer's disease (AD) has been demonstrated in several studies. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
MpHE efficiently reduced astrogliosis, the presence of insoluble Aβ peptides in the hippocampus and spatial learning impairments, of both, lean, and obese 5XFAD mice. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Redistribution of the water channel aquaporin-4 (AQP4) away from astrocyte endfeet and into parenchymal processes is a striking histological feature in mouse models of Alzheimer's disease (AD) and other neurological conditions with prominent astrogliosis. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
CSF can be stored for up to 72 h at RT, 1 week at 4 °C, or at least 2 weeks at either - 20 °C or - 80 °C before Aβ measurements. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our results suggest that the mechanism underlying low CSF Aβ levels differs between amyloid PET(-) iNPH and amyloid PET(+) AD subjects. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Detection of amyloid-β (Aβ) aggregates contributes to the diagnosis of Alzheimer disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Cognitive deficits exhibited by FAD rats were not exacerbated by the introduction of the SHRSP phenotype, nor was the hyperactivity phenotype associated with SHRSP altered by the FAD transgene. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Among mediators of inflammation, chemokines play a pivotal role in the neuroinflammatory process related to Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) and atherosclerosis are both chronic age- and inflammation-dependent diseases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Significant differences between platelet characteristics from AD patients and HC at the time of first clinical diagnosis were observed. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Much testing in medicine is aimed at healthy people to facilitate the early detection of health conditions. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Given the importance of early diagnosis of AD patients, it was suggested that the measurement of plasma levels and also mRNA expression of BACE1 might be a valuable blood-based biomarker used in preference to other invasive diagnostic methods such as cerebrospinal fluid (CSF) analysis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Activated Caspase-6 (Casp6) is associated with age-dependent cognitive impairment and Alzheimer disease (AD). 2 key findings →
Evidence: low
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
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
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 31,780 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 31,780 records, built mostly from automated pulls of Europe PMC (66% of the library) and OpenAlex (16%), 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.
1,052 records (3.3% of the library) are not peer-reviewed — 973 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events