27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Reduced hippocampal volumes are probably the most frequently reported structural neuroimaging finding associated with major depressive disorder (MDD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We compared hippocampal volume measures obtained by manual tracing to automatic segmentation with FreeSurfer in 44 younger (20-30 years) and 47 older (60-70 years) adults, each measured with magnetic resonance imaging (MRI) over three successive time points, separated by four months. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
(18)F-THK523 does not bind to Aβ in vivo, while following the known distribution of paired helical filaments (PHF)-tau in the brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The Notch signalling pathway is evolutionarily conserved and is crucial for the development and homeostasis of most tissues. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Low-to-moderate red wine consumption appeared to reduce age-related neurological disorders including macular degeneration, stroke, and cognitive deficits with or without dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The close relationship between stroke and dementia is an important health issue. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The discovery that the apolipoprotein E (apoE) ε4 allele is genetically linked to both sporadic and familial late-onset Alzheimer's disease (AD) raises the possibility that a dysfunction of the lipid transport system could seriously affect lipid homeostasis in the brain of AD subjects. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In sporadic Alzheimer's disease (AD), impaired Aβ removal contributes to elevated extracellular Aβ levels that drive amyloid plaque pathogenesis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Melatonin acts as a pleiotropic agent in various age-related neurodegenerative diseases. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Several studies have highlighted the frequency of sleep disturbances in Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The presenilin-containing γ-secretase complex produces the amyloid β-peptide (Aβ) through intramembrane proteolysis, and >100 presenilin mutations are associated with familial early-onset Alzheimer disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
It has been estimated that Alzheimer's disease (AD), the most common form of dementia, will affect approximately 81 million individuals by 2040. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Worse pain scores and executive function scores were associated with worse physical function in older adults with painful knee OA. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Apolipoprotein (apo) E is a multifunctional protein with central roles in lipid metabolism, neurobiology, and neurodegenerative diseases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Among the three human apolipoprotein E (apoE) isoforms, apoE4 increases the risk of Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a clinically heterogeneous neurodegenerative disease with a strong genetic component. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mitochondria form a highly interconnected tubular network throughout the cell via a dynamic process, with mitochondrial segments fusing and breaking apart continuously. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
What can be expected in normal aging, and where does normal aging stop and pathological neurodegeneration begin? 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Brain stimulation, a therapy increasingly used for neurological and psychiatric disease, traditionally is divided into invasive approaches, such as deep brain stimulation (DBS), and noninvasive approaches, such as transcranial magnetic stimulation. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Functional connectivity (FC) sheds light on the interactions between different brain regions. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Normal aging and Alzheimer's disease (AD) cause profound changes in the brain's structure and function. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Astrocyte activation and reactive gliosis accompany most of the pathologies in the brain, spinal cord, and retina. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Structural and functional connectivity methods are changing how researchers conceptualize and explore neuropsychiatric disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent trials of anti-amyloid agents have not produced convincing improvements in clinical outcome in Alzheimer's disease; however, the reason for these poor or inconclusive results remains unclear. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative disease is one of the greatest health crises in the world and as life expectancy rises, the number of people affected will continue to increase. 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 →