The presubiculum captures unique AD-related biological variation that is not reflected in total hippocampal volume. 2 key findings →
Participants: 127 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
The presubiculum captures unique AD-related biological variation that is not reflected in total hippocampal volume. 2 key findings →
Participants: 127 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Late-onset Alzheimer's disease (AD) is 50-70% heritable with complex genetic underpinnings. 4 key findings →
Participants: 104 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These findings support the idea that vascular amyloid burden directly contributes to chronic cerebral ischemia and highlights the possible utility of amyloid imaging as a marker of CAA severity. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These results demonstrate that temporoparietal regions show differential rates of atrophy on MRI during prodromal Alzheimer disease (AD). 5 key findings →
Participants: 66 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a progressive age-related neurodegenerative disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Executive predominant AD may reflect an alternative underlying pathophysiology related to genetic status, reflected in more prominent pathological alterations in frontoparietal regions subserving executive function. 2 key findings →
Participants: 100 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The Alzheimer's Disease Neuroimaging Initiative (ADNI) is a large multi-center study designed to develop optimized methods for acquiring longitudinal neuroimaging, cognitive, and biomarker measures of AD progression in a large cohort of patients with Alzheimer's disease (AD), patients with Mild Cognitive Impairment, and healthy controls. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These results suggest a potential link between vascular risk and tau pathology in preclinical AD. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) neuropathology is extremely heterogeneous, and the evolution from preclinical to mild cognitive impairment until dementia is driven by interacting genetic/biological mechanisms not fully captured by current clinical/research criteria. 2 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We report the clinical, neuroimaging, and neuropathologic characteristics of 2 patients who developed early onset dementia after a moderate-severe traumatic brain injury (TBI). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The study of Alzheimer's disease (AD), the most common cause of dementia, faces challenges in terms of understanding the cause, monitoring the pathogenesis, and developing early diagnoses and effective treatments. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
O]water PET were strongest for 1800 msec single-PLD and generally decreased with longer PLDs, except the occipital lobe, where all PLDs showed poor agreement. 5 key findings →
Design: longitudinal study Evidence: moderate
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White matter hyperintensities (WMH) are neuroimaging markers linked to an elevated risk of cognitive decline. 2 key findings →
Participants: 60 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Noninvasive quantitative approaches provide valid estimates of amyloid-β binding. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Adults with Down syndrome (DS) have an exceptionally high prevalence of Alzheimer disease (AD), with an earlier age of onset compared with the neurotypical population. 4 key findings →
Participants: 339 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
For prediction of dementia in MCI, the AD signature cortical thickness biomarker performed better than hippocampal volume. 3 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
25 older individuals with MCI performed a visual scene encoding task during fMRI scanning, and were followed clinically for at least 4 years after scanning. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Disorders associated with early-life alterations in amyloid precursor protein production or processing are associated with a distinct pattern of early striatal fibrillary Aβ deposition before significant cognitive impairment. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Converging evidence suggests that accumulation may be driven by spreading through network connections and/or interactions with amyloid-β (Aβ). 2 key findings →
Participants: 522 Evidence: low
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We found 5 distinct clusters of subjects (N=38, N=16, N=24, N=14, N=21) with a composition statistically independent from that obtained using available clinical diagnostic criteria (each cluster included all phenotypical groups). 3 key findings →
Participants: 20 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
By age 40 years over 90% of adults with Down syndrome (DS) have Alzheimer’s disease (AD) pathology and most progress to dementia. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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 →