Alzheimer's disease (AD) is a neurodegenerative disorder, the most common form of dementia. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
The progressive aging of the population will notably increase the burden of those diseases which leads to a disabling situation, such as Alzheimer's disease (AD) and ophthalmological diseases that cause a visual impairment (VI). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
There is consistent evidence that dementia affects driving ability. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Detailed analyses of neuronal and astrocyte cell numbers in the ganglion cell layer (GCL) of whole-mounted peripheral retinas from 16 Alzheimer's disease (AD) and 11 control eyes (11 and 9 cases, respectively) demonstrate extensive neuronal loss throughout the entire retina in AD as compared to control eyes. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The earliest detectable change in Alzheimer's disease (AD) is the buildup of amyloid plaque in the brain. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Optic nerve and retinal ganglion cell (GC) degeneration are possible explanations for the poor visual function reported in patients with Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In patients with Alzheimer's disease (AD), compared with age-matched and young healthy control subjects, visual deficits in the following functions were observed: color, stereoacuity, contrast sensitivity, and backward masking (homogeneous and pattern). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Ophthalmologic abnormalities have been described in patients with dementia, but the extent to which poor vision and treatment for visual disorders affect cognitive decline is not well defined. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Optical Coherence Tomography Angiography (OCTA) is a non-invasive imaging technique that has been increasingly used to image the retinal vasculature at capillary level resolution. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Optical coherence tomography (OCT) is a well-established technique for the clinical examination, diagnosis, severity staging and monitoring of ophthalmic disorders. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Retinal microcirculation shares similar features with cerebral small blood vessels. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Visual dysfunction has long been recognized as a manifestation of Alzheimer's disease (AD), particularly in the form of visuospatial impairment during all stages of disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
Spectral-domain optical coherence tomography (SD-OCT) is an accessible clinical tool for measuring structural changes to the retina, and increasingly as a biomarker for brain-predominant neurodegenerative diseases like Alzheimer's. Information about retinal function can also be extracted from OCT images, but is under-studied, with literature examples often employing challenging protocols or requiring specialized hardware. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The retina offers a unique "window" to study pathophysiological processes of dementia in the brain, as it is an extension of the central nervous system (CNS) and shares prominent similarities with the brain in terms of embryological origin, anatomical features and physiological properties. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In diabetic retinopathy, venous oxygen saturation increases and arteriovenous difference decreases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The ensuing upward shift in demographic distribution due to the increase in life expectancy has resulted in a rising prevalence of Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In terms of the retinal neuronal structure, multiple retinal neuronal layers are significantly thinner in Alzheimer's disease dementia, such as the parapapillary retinal nerve fiber layer (RNFL) and macular ganglion cell-inner plexiform layer (GC-IPL). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
It could be shown that Alzheimer type dementia, Parkinson's disease, multiple sclerosis. cerebral infarction and CADASIL are neuronal diseases with rarification of retinal vessels and atrophy of the retinal layers in the ocular fundus. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
There was a significant increase in the total number of macular and peripheral hard drusen in older, compared to younger, normal eyes (p<0.05). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The main advantages of optical retinal imaging may allow researchers to achieve deeper analysis of retinal ganglion cells (GC) in vivo using optical coherence tomography (OCT). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
39/100
OCTA has been applied in research to advance our understanding of the pathobiology of neurological disorders. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Interest in reliable biomarkers of Alzheimer disease, the leading cause of dementia, has been fuelled by challenges in diagnosing the disease and monitoring disease progression as well as the response to therapy. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Age-related cataracts are frequently associated with degenerative changes in the ocular lens including the aggregation of proteins - mainly crystallins, but also other proteins including amyloids (Aβ) leading to the hypothesis that cataracts could be used as "biomarkers" for Alzheimer disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Central nervous system (CNS) pathologies have ocular manifestations due to direct and/or retrograde degeneration of the visual pathways, most often related to a direct injury to the optic nerve, retinal ganglion cells and/or its surrounding cells. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a devastating neurodegenerative disease characterised clinically by a progressive decline in executive functions, memory and cognition. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
7 of the 151 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 7. The same 7 appear here every time.
- Dll4 signalling through Notch1 regulates formation of tip cells during angiogenesis
- The Eye as a Diagnostic Tool for Alzheimer's Disease
- Optic-nerve degeneration in Alzheimer's disease
- Retinal ganglion cell analysis using high-definition optical coherence tomography in patients with mild cognitive impairment and Alzheimer's disease
- Mechanisms of lower oesophageal sphincter incompetence in patients with symptomatic gastrooesophageal reflux
- Retinal imaging in Alzheimer's disease
- Retinal biomarkers and dementia risk: A review of evidence across the 14 Lancet modifiable risk factors for dementia
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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 (3.7% 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 →