27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Several magnetic resonance imaging studies have reported hippocampal volume reduction in patients with schizophrenia, but other studies have reported contrasting results. 2 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Our findings reveal that specific gut microbial features are closely associated with cognitive impairment and decreased hippocampal volume, which may play an important role in dementia development. 4 key findings →
Design: case-control study Participants: 90 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Memory decline accompanies Aβ accumulation in otherwise healthy, Aβ-negative older adults. 3 key findings →
Design: longitudinal study Participants: 13 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Previous studies in humans have shown the presence of an age-related reduction of hippocampal (HC) volume, as well as the presence of reduced HC volume in psychiatric populations suffering from schizophrenia, depression or post-traumatic stress disorder. 3 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
Metabolic dysregulation, especially insulin resistance, was associated with lower brain volumes and executive function in a large, relatively healthy, middle-aged, community-based cohort. 3 key findings →
Design: cross-sectional Participants: 2,439 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Fornix body volume and axial diffusivity were highly significant predictors (P = .02 and .005, respectively) of cognitive decline from normal cognition. 3 key findings →
Design: longitudinal study Participants: 102 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The consistency of MRI measurements obtained across sites, and the consistency between the multisite milameline data and that obtained in prior single-site studies, demonstrate the technical feasibility of using structural MRI measures as a surrogate endpoint of disease progression in therapeutic trials. 1 key finding →
Participants: 362 Evidence: high
Full summary, score breakdown and related studies → Original source
Previous animal models and structural imaging investigations have linked hippocampal neuroplasticity to electroconvulsive therapy (ECT) response, but the relationship between changes in hippocampal volume and temporal coherence in the context of ECT response is unknown. 2 key findings →
Design: longitudinal study Participants: 19 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alterations in the hippocampus were evident across psychotic disorders. 2 key findings →
Design: case-control study Participants: 219 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Structural imaging studies investigating hippocampal volumes in patients suffering from major depression have yielded mixed results. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The hippocampus has been shown to demonstrate a remarkable degree of plasticity in response to a variety of tasks and experiences. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Complaints of poor memory by older people, particularly when new, may be a realistic subjective appraisal of recent brain changes independent of observed cognitive decline. 2 key findings →
Design: cohort study Participants: 1,336 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The results suggest that longitudinal structural trajectories may differ in major depressive disorder patients according to their clinical response to treatment. 4 key findings →
Design: longitudinal study Participants: 26 Evidence: moderate
Full summary, score breakdown and related studies → Original source
(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
Although numerous studies of the longitudinal course of schizophrenia have demonstrated the clinical deterioration that occurs predominantly in the early stages of the illness, the pathophysiology of this clinical phenomenon has not been established. 5 key findings →
Design: longitudinal study Participants: 107 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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
A larger WHR may be related to neurodegenerative, vascular, or metabolic processes that affect brain structures underlying cognitive decline and dementia. 3 key findings →
Design: cohort study Participants: 112 Evidence: moderate
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
Odor identification deficits occur in Alzheimer's disease (AD) and mild cognitive impairment (MCI), and predict clinical conversion from MCI to AD. 4 key findings →
Design: longitudinal study Participants: 571 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We investigated in a population-based cohort study the association of global and lobar brain tissue volumes with specific cognitive domains and risk of dementia. 3 key findings →
Design: cohort study Participants: 490 Evidence: moderate
Full summary, score breakdown and related studies → Original source
To explore neural correlates of cognitive decline in aging, we used longitudinal behavioral data to identify two groups of older adults (n = 40) that differed with regard to whether their performance on tests of episodic memory remained stable or declined over a decade. 4 key findings →
Design: longitudinal study Participants: 40 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
Models combining multiple risk factors should refine the prediction of questionable dementia and persistent cognitive impairment, harbingers of dementia. 4 key findings →
Design: cohort study Participants: 48 Evidence: moderate
Full summary, score breakdown and related studies → Original source
These findings highlight the diagnostic and longitudinal monitoring potential of GFAP and p-tau for preclinical AD. 5 key findings →
Design: longitudinal study Evidence: moderate
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 →