Our results demonstrate that tau, not amyloid, was associated with a depression diagnosis. 5 key findings →
Participants: 301 Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Atlas normalization, as commonly used by functional data analysis, provides an automated solution to the widely encountered problem of correcting for head size variation in regional and whole-brain morphometric analyses, so long as an age- and population-appropriate target atlas is used. 2 key findings →
Participants: 49 Evidence: low
Full summary, score breakdown and related studies → Original source
Rates of hippocampal volume loss have been shown to distinguish subjects with dementia of the Alzheimer type (DAT) from nondemented controls. 3 key findings →
Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source
Assessments of hippocampal volume and shape derived from HDBM may be useful in distinguishing early DAT from healthy aging. 2 key findings →
Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source
47/100
Reduction in CSF Abeta(42), likely reflecting Abeta aggregation in the brain, is associated with brain atrophy in the preclinical phase of AD. 3 key findings →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source
These results are supportive of an association between exercise engagement and AD biomarkers in cognitively normal older adults. 5 key findings →
Participants: 56 Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer disease (AD) and Alzheimer Disease and Related Dementias (AD/ADRD) are growing public health challenges globally affecting millions of older adults, necessitating concerted efforts to advance our understanding and management of these conditions. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Biomarkers are needed to improve the sensitivity and accuracy of diagnosis, and also prognosis, in individuals with early Alzheimer disease (AD). 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
These findings suggest that NfL can be used to monitor cognitive decline in aging and Alzheimer's disease and that an attentional control composite may be a better outcome for tracking general neurodegenerative effects on cognition. 3 key findings →
Participants: 255 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Since the original publication describing the illness in 1907, the genetic understanding of Alzheimer's disease (AD) has advanced such that it is now clear that it is a genetically heterogeneous condition, the subtypes of which may not uniformly respond to a given intervention. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Dementia adversely affects driving performance even in its mild stages, although some persons with DAT seem to drive safely for some time after disease onset. 1 key finding →
Participants: 123 Evidence: low
Full summary, score breakdown and related studies → Original source
Controversy persists regarding whether Alzheimer's disease (AD) is a distinct entity or instead exists on a continuum with nondemented aging. 5 key findings →
Participants: 150 Evidence: low
Full summary, score breakdown and related studies → Original source
These results suggest that cognitively normal sedentary APOE ε4-positive individuals may be at augmented risk for cerebral amyloid deposition. 5 key findings →
Participants: 165 Evidence: low
Full summary, score breakdown and related studies → Original source
Recent functional magnetic resonance imaging studies have demonstrated that moment-to-moment variability in the blood oxygen level-dependent (BOLD) signal is related to age differences, cognition, and symptomatic Alzheimer's disease (AD). 1 key finding →
Participants: 321 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is the leading cause of dementia, accounting for 60-70% of all cases [Hebert et al., 2003, 1]. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Before any manifestations of cognitive or behavioral changes, there were differences in resting state connectivity in cognitively normal subjects with brain amyloid deposition, suggesting that early manifestation of Abeta toxicity can be detected using resting state fMRI. 3 key findings →
Participants: 35 Evidence: low
Full summary, score breakdown and related studies → Original source
Because even the very mildly demented brains showed substantial pathological change, emphasis was placed on examining the nondemented cases for the earliest changes that could be associated with Alzheimer's disease. 2 key findings →
Participants: 13 Evidence: low
Full summary, score breakdown and related studies → Original source
Change detected by the MCI-CGIC was associated with baseline clinical severity and with change in clinical ratings over 6 and 12 months, supporting the validity of a CGIC approach in MCI. 5 key findings →
Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
We studied the validity of longitudinal statistical inferences of clinical trials using minimization, a dynamic randomization algorithm designed to minimize treatment imbalance for prognostic factors. 1 key finding →
Design: longitudinal study Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Preclinical AD risk, defined as possessing at least one APOE ε4 allele, is not only associated with mean-level performance differences, but also with increases in variability across repeated testing occasions particularly on a test of processing speed. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Assay drift may reduce statistical power or even confound analyses. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) pathology is estimated to develop many years before detectable cognitive decline. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The value of screening for cognitive impairment, including dementia and Alzheimer's disease, has been debated for decades. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
40/100
The expression levels of three synaptic proteins (synaptophysin, synaptotagmin, and growth-associated protein 43 [GAP43]) in AD cases clinically classified by Clinical Dementia Rating (CDR) score were analyzed. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The modified questionnaire and interview instruments capture a range of impairment in DS adults, including subthreshold symptomatology, and the instruments provide complementary information relevant to the ascertainment of dementia in DS. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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 28,580 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.
What this library is — and isn't
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →