27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Studies suggest that n-3 fatty acids in the diet and adherence to the MedDiet are beneficial in slowing age-related cognitive decline. 5 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Sarcopenia is highly prevalent in individuals with CVD, dementia, diabetes mellitus and respiratory disease. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Slow gait speed has been shown to predict incident dementia and cognitive decline in older individuals. 1 key finding →
Design: longitudinal study Participants: 57,456 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A study with a more intensive multidomain intervention might bring further insights on this topic. 3 key findings →
Participants: 1,679 Evidence: high
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Glial fibrillary acidic protein (GFAP) and neurofilament light (NfL) are putative non-amyloid biomarkers indicative of ongoing inflammatory and neurodegenerative disease processes. 2 key findings →
Participants: 20 Evidence: moderate
Full summary, score breakdown and related studies → Original source
To examine the association between dietary habits, cognitive functioning and brain volumes in older individuals, data from 194 cognitively healthy individuals who participated in the Prospective Investigation of the Vasculature in Uppsala Seniors cohort were used. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Among 157 subjects with a mean age of 71.8 (±7.7) included in this study, 76 individuals were stratified as metformin users. 5 key findings →
Participants: 157 Evidence: low
Full summary, score breakdown and related studies → Original source
During aging, there is a progressive impairment of immune cell function that triggers the production of pro-inflammatory cytokines causing the so-called “inflammaging”. 3 key findings →
Participants: 235 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
After adjusting for potential confounders, multivariable logistic regression models revealed that the prevalence of dementia was significantly higher in individuals with chronic pain than in those without. 3 key findings →
Design: cross-sectional Participants: 1,096 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The importance of (micro)vascular contributions to cognitive impairment and dementia (VCID) in aging cannot be overemphasized, and the pathogenesis and prevention of age-related cerebromicrovascular pathologies are a subject of intensive research. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Lesions in such chronic neurodegenerative disorders as Alzheimer disease (AD), Parkinson disease, the parkinsonism dementia complex of Guam, and amyotrophic lateral sclerosis have associated with them a variety of proteins known to be involved in inflammatory processes. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Postoperative cognitive dysfunction (POCD) is a common disorder following surgery, which seriously threatens the quality of patients' life, especially the older people. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Mild cognitive impairment (MCI) associated with physical frailty gave rise to the new concept of cognitive frailty. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The normal on and off switching of the PI3-K (phosphoinositide 3-kinase)/Akt pathway, particularly by its major activators insulin and IGF-1 (insulin-like growth factor-1), is a powerful integrator of physiological responses rudimentary to successful aging. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Active immunization with the human amyloid peptide (Abeta42) or passive immunization with anti-Abeta42 antibodies protects mice that express a mutant human amyloid precursor protein (APP) transgene from cerebral amyloid deposits. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The worldwide burden of dementia is immense, and set to increase to unprecedented levels in the coming decades, due to population aging. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Frailty syndrome encompasses several physical hallmarks such as loss of muscle strength, power output and mass, which leads to poor gait ability, fatigue, falls and overall difficulty to perform activities of daily living. 1 key finding →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source
It has been suggested that exercise training and probiotic supplementation could decelerate the progress of functional and biochemical deterioration in APP/PS1 transgenic mice (APP/PS1 TG ). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Advances in our understanding of tau-mediated neurodegeneration in Alzheimer's disease (AD) are moving this disease pathway to center stage for the development of biomarkers and disease modifying drug discovery efforts. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The senescence-accelerated mouse (SAM) is an accelerated aging model that was established through phenotypic selection from a common genetic pool of AKR/J strain of mice. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The circadian rhythm of the pineal gland hormone, melatonin is generated within the hypothalamic suprachiasmatic nuclei (SCN), site of the circadian clock. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We tested here the impact of a long-term inhibition of dipeptidyl peptidase-4 (DPP-4) with sitagliptin on the deposition of amyloid-beta within the brain and deficits in memory-related behavioral paradigms in a model of Alzheimer's disease (AD): double transgenic mice B6*Cg-Tg(APPswe,PSEN1dE9)85Dbo/J. Mice began to receive sitagliptin at 7 months of age. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Ageing is accompanied by 2-4-fold increases in plasma/serum levels of inflammatory mediators such as cytokines and acute phase proteins. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Evolutionary aspects of menopause are considered from several perspectives. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Immunocytochemical techniques was used to compare the proportion of neurons expressing various neurotransmitters (tyrosine hydroxylase, choline acetyltransferase and gamma-aminobutyric acid), neuropeptides (Leu-enkephalin and substance P) and neural cell adhesion molecules (NCAM) in the hippocampus, frontal (area 10) and occipital (area 17) cortices of neurologically normal elderly humans to that of age-matched Alzheimer disease (AD) patients. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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 →