27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Research is needed with methodologically rigorous designs and theoretical frameworks that examine cognitive, psychosocial, and environmental factors influencing ACP attitudes, preferences, and behaviors among PWDs in order to improve engagement among this population. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Astrocytic contributions to Alzheimer's disease (AD) progression were, until recently, largely overlooked. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Hesperetin is a bioactive flavonoid in the body, produced from hesperidin. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Multiplex immunoassay conducted on brain lysates showed that alcohol drinking upregulated primary markers of AD pathology in 3xTg-AD mice: Aβ 42/40 ratio in the lateral entorhinal and prefrontal cortex and total Tau expression in the lateral entorhinal cortex, medial prefrontal cortex, and amygdala at 1-month post alcohol exposure. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Blood-based diagnosis (hemodiagnosis) of Alzheimer's disease (AD) is emerging as a promising alternative to cerebrospinal-fluid-based methods because blood contains various kinds of AD biomarkers, including amyloid beta 1-40, 1-42, and τ (tau) protein. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
As we age, we experience changes in our nighttime sleep and daytime wakefulness. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The global epidemic of Alzheimer disease (AD) is worsening, and no approved treatment can revert or arrest progression of this disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is considered a polygenic disorder. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Prediction of disease risk is an essential part of preventative medicine, often guiding clinical management. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) has a very strong genetic component, whose characterization has become an essential part of efforts to understand the pathophysiological processes of the disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Among the changes that typify Alzheimer's disease (AD) are neuroinflammation and microglial activation, amyloid deposition perhaps resulting from compromised microglial function and iron accumulation. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglia, the brain-resident immune cells, are critically involved in many physiological and pathological brain processes, including neurodegeneration. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Familial Alzheimer's disease (fAD) results from mutations in the amyloid precursor protein (APP) and presenilin (PSEN1 and PSEN2) genes. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Complement pathway overactivation can lead to neuronal damage in various neurological diseases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Antisense oligonucleotides represent a novel therapeutic platform for the discovery of medicines that have the potential to treat most neurodegenerative diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) has been a global concern for years due to its severe implications that affects the quality of life of the patients. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most prevalent form of dementia, particularly in old age subjects. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is closely related to gut microbial alteration. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Glucose-dependent Insulinotropic polypeptide (GIP) is a peptide hormone of the incretin family. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Dulaglutide, a novel long-acting glucagon-like peptide 1 (GLP-1) receptor agonist, is an incretin mimetic approved for type 2 diabetes mellitus (T2DM) treatment. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Glucagon-like peptide-1 (GLP-1) signaling in the brain plays an important role in the regulation of glucose metabolism, which is impaired in Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The role of mitochondrial dysfunction has been well-documented in Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The current absence of effective treatments for Alzheimer's disease (AD) and Parkinson's disease (PD) reflects an incomplete knowledge of the underlying disease processes. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
These data suggest that the neuroprotective effects of liraglutide on diabetes-induced cognitive impairments are associated with the improvements of hippocampal synapses and inhibition of neuronal apoptosis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The foundation of current Alzheimer's disease (AD) treatment involves pharmacological and nonpharmacological management and care planning predicated on patient-centered psychoeducation, shared goal-setting, and decision-making forged by a strong triadic relationship between clinician and the patient-caregiver dyad. 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 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 →