27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
The AD PRS was associated with AD in the ADSP sample, with odds ratios per standard deviation ranging from 1.14 to 1.52 across ancestry groups and robust validation in independent cohorts (Figure 1). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer Disease (AD) is a highly polygenic dementia that presents with relatively earlier onset (≤65yo; EOAD) in about 5% of cases. 2 key findings →
Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
BackgroundTo date, cholinomimetics remain central in the pharmacotherapy of Alzheimer's disease (AD) dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The CU- group had lower baseline GAP-43 than all Aβ+ groups, but not the other Aβ- groups. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer?s disease (AD) is a neurodegenerative disorder with a strong genetic component. 4 key findings →
Design: case-control study Participants: 98 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In the AD and non-AD group, OEF showed negative associations with WMH in DGM and positive associations with MoCA in DGM and CGM. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD), the most prevalent form of dementia, is neuropathologically defined by the accumulation of extracellular amyloid-beta (Aβ) plaques and intracellular neurofibrillary tangles of hyperphosphorylated tau. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
APP/PS1 mice at 6 months were randomly allocated to two dietary groups: one receiving ad libitum (AL) feeding and the other undergoing IF for 1 month. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Alzheimer's Disease (AD), the most common form of dementia, is pathologically defined by extracellular beta-amyloid (Aβ) plaques and intraneuronal neurofibrillary tangles (NFTs), accompanied by chronic neuroinflammation. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer’s disease (AD) is the most prevalent cause of dementia, characterized by progressive cognitive decline, amyloid-β (Aβ) plaques, and neurofibrillary tangles composed of hyperphosphorylated tau protein. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The study of Alzheimer's disease (AD)-associated mutations has implicated dysregulation of amyloid precursor protein (APP) proteolysis in the disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD), the most prevalent form of dementia, is characterized by hallmark pathologies such as amyloid-beta (Aβ) plaque accumulation, tau hyperphosphorylation, and progressive neuronal dysfunction. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Socioeconomic disadvantage (SED) has been associated with poorer brain health, yet its underlying pathology remains incompletely understood. 5 key findings →
Participants: 1,110 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease currently has no cure and is usually detected too late for interventions to be effective. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
It is increasingly accepted that early cognitive impairment in Alzheimer's disease results in considerable part from synaptic dysfunction caused by the accumulation of a range of oligomeric assemblies of amyloid β-protein (Aβ). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The apolipoprotein E ( APOE ) ε4 allele is the strongest genetic risk factor for late-onset Alzheimer's disease mainly by driving amyloid-β pathology. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In normal brain, neurons in the cortex and hippocampus produce insulin, which modulates glucose metabolism and cognitive functions. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Melatonin, a pineal gland synthesized neurohormone is known as a multifunctioning pleiotropic agent which has a wide range of neuroprotective role in manifold age-related neurodegenerative disorders especially Alzheimer's diseases (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In Alzheimer's disease (AD), insoluble and fibrillary amyloid-β (Aβ) peptide accumulates in plaques. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by the presence of amyloid-β (Aβ), oxidative damage and neuronal degeneration, which, together with other pathological events, promote progressive memory loss and cognitive decline. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common cause of dementia, and its prevalence will increase significantly in the coming decades. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Congo Red (CR) has been used for its binding affinity to amyloid fibrils for the better part of a century. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Transcriptional regulation of the gene encoding the amyloid precursor protein (APP) may play an important role in the formation of the amyloid depositions observed in Alzheimer disease and Down syndrome patients. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
The vascular and parenchymal amyloid deposits in Alzheimer disease (AD), normal aging and Down syndrome are mainly composed of a 4 kDa polypeptide (A4), which derives from a larger precursor protein (APP). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The molecular mechanisms of beta-amyloidogenesis in sporadic Alzheimer's disease are still poorly understood. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
10 of the 1,344 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →