(1) Data-driven AD progression models supported multifactorial interactions rather than a linear cascade of events. 4 key findings →
Design: longitudinal study Evidence: high
Full summary, score breakdown and related studies → Original source
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
(1) Data-driven AD progression models supported multifactorial interactions rather than a linear cascade of events. 4 key findings →
Design: longitudinal study Evidence: high
Full summary, score breakdown and related studies → Original source
The findings indicate for the first time in humans that PTSD is associated with selective volume loss of the CA3/dentate gyrus subfields, consistent with animal studies, implying that chronic stress suppresses neurogenesis and dendritic branching in these structures. 4 key findings →
Design: case-control study Participants: 17 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Trajectories of Aβ42 level in CSF, FDG uptake, and hippocampal volume vary across different cognitive stages. 3 key findings →
Design: cohort study Participants: 819 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer disease-specific cortical thinning and hippocampal volume loss are consistent with a sigmoidal pattern, with an acceleration phase during the early stages of the disease. 2 key findings →
Design: case-control study Participants: 317 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Hippocampal volume may index disease severity and predict progression in AD. 4 key findings →
Design: cross-sectional Participants: 120 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Compared with healthy controls, adults with SCA had poorer cognitive performance, which was associated with anemia and age. 3 key findings →
Design: cross-sectional Participants: 149 Evidence: low
Full summary, score breakdown and related studies → Original source
Mild cognitive impairment can represent a transitional state between normal ageing and Alzheimer's disease. 4 key findings →
Participants: 49 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Subcortical lacunes were not related to cognitive measures independent of effects of other MRI variables. 3 key findings →
Participants: 157 Evidence: low
Full summary, score breakdown and related studies → Original source
Cross-sectional studies of normal aging indicate an association between memory and hippocampal volume, and between executive functioning and subcortical-frontal circuits. 3 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
The pattern of thinning in TLE-no was different from the pattern in TLE-MTS. 3 key findings →
Participants: 66 Evidence: low
Full summary, score breakdown and related studies → Original source
The cornu ammonis 1 region of the hippocampus (CA1) sector of hippocampus is vulnerable to both Alzheimer's disease (AD)-type neurofibrillary degeneration and anoxia-ischemia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
N-acetyl asparate and creatine reductions imply that there are hippocampal abnormalities in posttraumatic stress disorder. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Magnetic resonance imaging (MRI) studies have produced controversial results concerning the correlation of hippocampal volume loss with increasing age. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The patterns of subfield atrophy in AD and MCI were consistent with patterns of neuronal cell loss/reduced synaptic density described by histopathology. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Because the automatic calculations were faster and less susceptible to rater bias than manual tracing, this automated method is expected to be very useful for analyzing hippocampal changes in studies of aging and dementia. 2 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 →