27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
At 48 months, group differences between clinical progressors and non-progressors were significant for self (2.13, SE=0.45, P Conclusions and relevance Demonstrating long-term clinical benefit will be critical for the success of recently launched secondary prevention trials. 1 key finding →
Design: longitudinal study Participants: 468 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Both participant and study partner CFI increased over the duration of the study indicating worsening cognitive functioning. 3 key findings →
Design: longitudinal study Participants: 1,147 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cross-sectional functional magnetic resonance imaging studies using a memory task in patients with mild cognitive impairment have produced discordant results, with some studies reporting increased hippocampal activity--consistent with findings in genetic at-risk populations--and other studies reporting decreased hippocampal activity, relative to normal controls. 3 key findings →
Design: cross-sectional Participants: 33 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Of 4413 individuals (mean [SD] age, 71.27 [4.66] years, 2617 women [59.3%]), mean Aβ-PET was elevated in individuals with history of memory impairment in both parents (n = 455; mean [SD] standardized uptake value ratio [SUVR] = 1.12 [0.19]; Wilcoxon P = 1.1 × 10-5) and in those with only maternal history (n = 1772; mean [SD] SUVR = 1.10 [0.19]; Wilcoxon P = 2.70 × 10-5) compared with those with only paternal history (n = 632; mean [SD] SUVR = 1.08 [0.18]; Wilcoxon P = 1.1 × 10-5) or no family history (n = 1554; mean [SD] SUVR = 1.08 [0.19]; Wilcoxon P = 1.1 × 10-5). 3 key findings →
Design: cross-sectional Participants: 455 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Loneliness is a perceived state of social and emotional isolation that has been associated with cognitive and functional decline and an increased risk of incident AD dementia. 5 key findings →
Design: cross-sectional Participants: 25 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Animal models of Alzheimer's disease have suggested that tau pathology propagation, facilitated by amyloid pathology, may occur along connected pathways. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The co-occurrence of Aβ and ND accelerates cognitive decline in CN individuals. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Accounting for educationalfactors, vascular factors, and Aβ burden diminished, but did not eliminate, racial differences in PACC5 performance longitudinally. 4 key findings →
Design: longitudinal study Participants: 296 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Although Aβ did not differ by sex, cognitive decline was greater in females with higher Aβ. 3 key findings →
Participants: 755 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Overall, individuals improved on all C3 measures over 12 months (β = 0.23, 95% CI [0.21-0.25], p < 0.001), but improvement over the first 3 months was greatest (β = 0.68, 95% CI [0.59-0.77], p < 0.001), suggesting stronger PE over initial repeated exposures. 4 key findings →
Participants: 114 Evidence: low
Full summary, score breakdown and related studies → Original source
From a total sample of 559 older adults from the Massachusetts Alzheimer's Disease Research Center longitudinal cohort, 454 were included in the primary analysis: 283 with clinically normal cognition (CN), 115 with mild cognitive impairment (MCI), and 56 with subjective cognitive concerns (SCC) but no objective impairment, a proposed transitional group between CN and MCI. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our objective was to investigate cross-sectional associations between odor identification ability and imaging biomarkers of neurodegeneration and amyloid deposition in clinically normal (CN) elderly individuals, specifically testing the hypothesis that there may be an interaction between amyloid deposition and neurodegeneration in predicting odor identification dysfunction. 1 key finding →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cerebral amyloid beta (Aβ) deposition occurs in a substantial fraction of cognitively normal (CN) older individuals. 3 key findings →
Participants: 45 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Older adults with subjective cognitive decline (SCD) in the absence of objective neuropsychological dysfunction are increasingly viewed as at risk for non-normative cognitive decline and eventual progression to Alzheimer's disease (AD) dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
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
Research increasingly suggests that subjective cognitive decline (SCD) in older adults, in the absence of objective cognitive dysfunction or depression, may be a harbinger of non-normative cognitive decline and eventual progression to dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Tau vulnerability in women is not just limited to the medial temporal lobe and significantly contributed to greater risk of faster cognitive decline. 2 key findings →
Participants: 55 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A decline in instrumental activities of daily living (IADL) correlates with the progression from mild cognitive impairment (MCI) to Alzheimer's disease (AD) dementia and has been associated with frontal and parietal hypometabolism, lower cerebrospinal fluid amyloid β 1-42 , and inferior temporal cortical thinning. 4 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Future longitudinal studies examining the association of more severe depressive symptoms and cerebral tau accumulation are needed to substantiate this finding and to guide prevention and treatment in AD. 4 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Excellent reliability was observed among the 6 C3-PAD alternate versions (Cronbach alpha coefficient=0.93). 5 key findings →
Participants: 49 Evidence: low
Full summary, score breakdown and related studies → Original source
Our results are consistent with the supposition that both Aβ and tau are necessary for memory decline in the preclinical stages of AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Accumulating evidence suggests that subjective cognitive complaints (SCC) may indicate subtle cognitive decline characteristic of individuals with preclinical Alzheimer's disease (AD). 4 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 →