27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Of 101 participants, 85 older adults without dementia (84.1%) who completed the study protocol were included in the statistical analysis. 5 key findings →
Participants: 51 Evidence: low
Full summary, score breakdown and related studies → Original source
A total of 1,350 publications with 59,818 citations were identified. 5 key findings →
Participants: 1,350 Evidence: low
Full summary, score breakdown and related studies → Original source
Thirteen pathway clusters were identified, and eight pathway-specific PRSs were significantly associated with AD diagnosis. 5 key findings →
Participants: 1,411 Evidence: low
Full summary, score breakdown and related studies → Original source
Polynomial regressions indicated an 0.23 kg/m2 decrease in BMI per year beginning at age 36.5 years, which occurs alongside the period during which Aβ and tau increase and memory and mental status decline. 3 key findings →
Participants: 77 Evidence: moderate
Full summary, score breakdown and related studies → Original source
There is greater interest in amyloid biomarker for the diagnosis of Alzheimer disease (AD) with the recent Food and Drug Administration approval of amyloid-targeted therapy. 1 key finding →
Participants: 74 Evidence: low
Full summary, score breakdown and related studies → Original source
Ninety-one eyes of AD patients and 53 eyes of patients with other dementias were included. 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
We found that AD cases with comorbid LATE-NC, AD(LATE-NC+), have increased burdens of pretangles and/or NFTs as well as increased brain levels of p-tau199, compared to AD(LATE-NC-) cases and controls. 5 key findings →
Participants: 98 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A total of 54.4% of the residents with dementia had been provided with information about their state of health, compared to 92.5% of the residents without dementia (p < 0.01); family members exhibited no differences regarding information (p = 0.658), regardless of whether the resident was cognitively impaired. 4 key findings →
Participants: 54 Evidence: low
Full summary, score breakdown and related studies → Original source
When considering race/ethnicity, the presence of more vascular comorbidities drove greater vulnerability. 4 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Neither HOMA-IR nor diabetic status was significantly associated with tau PET SUVR. 5 key findings →
Participants: 280 Evidence: low
Full summary, score breakdown and related studies → Original source
This study supports that PET- and CSF-related A/T/N profiles can be used to predict accurately the stages of AD neuropathology. 2 key findings →
Participants: 100 Evidence: low
Full summary, score breakdown and related studies → Original source
Among 455,306 UK Biobank participants, 37 carried one copy of the APOE Christchurch variant (allele frequency 0.004%). 4 key findings →
Design: cohort Participants: 455,306 Evidence: early
Full summary, score breakdown and related studies → Original source Free full text
After disclosure, 27 patients with amyloid-positive SCD+ (median [IQR] age, 70 [66-74] years; gender: 14 men [52%]; median [IQR] education: 15 [13 to 17] years, median [IQR] Mini-Mental State Examination [MMSE] score, 29 [28 to 30]) had higher median (IQR) IES-R total score (10 [2 to 14] vs 0 [0 to 2]; P Conclusions and relevance The disclosure of a positive amyloid-PET result to patients with SCD+ was associated with a bigger psychological change, yet such change did not reach the threshold for clinical concern. 5 key findings →
Participants: 27 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
There is growing evidence that cognitive decline can be affected by both nutritional aspects and inflammation. 3 key findings →
Design: cross-sectional Participants: 116 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Across 3 study samples, combining the functional connectome and molecular properties substantially enhanced the explanatory power compared to single modalities, providing a valuable tool to explain regional susceptibility to tau deposition in AD. 3 key findings →
Participants: 1,000 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The risk of Alzheimer disease (AD) increases with age, family history and informative genetic variants. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
These results highlight the need to increase the overall detection rates of MCI and of dementia particularly in socioeconomically disadvantaged groups. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
We still do not have an effective treatment for Alzheimer's disease (AD) despite it being the most common cause of dementia and impaired cognitive function. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Tumor cells promote the recruitment of immunosuppressive neutrophils, a subset of myeloid cells driving immune suppression, tumor proliferation, and treatment resistance. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Triggering receptor expressed on myeloid cells 2 (TREM2) is strongly linked to Alzheimer's disease (AD) risk, but its functions are not fully understood. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Triggering receptor expressed on myeloid cells 2 (TREM2) plays important roles in brain microglial function in neurodegenerative diseases, but the role of TREM2 in the GBM TME has not been examined. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Sleep loss is associated with cognitive decline in the aging population and is a risk factor for Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) remains one of the grand challenges facing human society. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
of 74,486 decedents (60.5% women; mean age 87.1 years (standard deviation: 7.1)), 82.6% had at least one ED visit in their last year of life. 3 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The 32 796 872 Medicare beneficiaries in the cohort had a mean (SD) age of 74.0 (12.5) years and included 18 228 513 females (55.6%). 5 key findings →
Design: cross-sectional Participants: 18 Evidence: moderate
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 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 →