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
Research
28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
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
Laboratory and epidemiological data indicate that high blood sugar levels and/or consuming high glycemia diets are linked to multiple age-related diseases, including age-related macular degeneration, cataract, Parkinson's disease, Alzheimer's disease, diabetic retinopathy, and, apparently glaucoma. 2 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
The recent failure of several clinical trials on anti-β-amyloid (Aβ) drugs in Alzheimer's disease (AD) suggested earlier intervention in the disease course. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Disease-modifying therapies for proteinopathies are urgently needed yet clinical trials for the major neurodegenerative diseases, Alzheimer's and Parkinson's, have been failing at an alarming rate leaving patients and caregivers scrambling for any sign of hope. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a progressive neurological disorder having two major pathological hallmarks: the extracellular senile plaques and intracellular neurofibrillary tangles composed of amyloid beta protein and hyperphosphorylated tau respectively. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of dementia. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease progressively impairs cognition and daily function, and death usually occurs five to ten years after diagnosis. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In contrast to the idea that tau phosphorylation is toxic, Ittner et al. (2016) recently showed that specific tau phosphorylation is neuroprotective, phenocopying tau ablation (DeVos et al., 2017), thus highlighting the complex tau biology that underlies neurotoxicity and neuroprotection. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Several neurodegenerative diseases, including amyotrophic lateral sclerosis (ALS), have a complex genetic background, in addition to cases where the disease appears to manifest sporadically. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Despite identification of many genes causing neurodegenerative diseases in the last decades, development of disease-modifying treatments has been slow. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Programmed cell death protein 1 (PD-1) checkpoint blockade with an antibody has been shown to reduce amyloid-β plaques, associated pathologies and cognitive impairment in mouse models. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Zinc is the second abundant trace element in the human central nervous system (CNS). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Efforts to develop effective disease-modifying treatments for Alzheimer's disease (AD) have mostly targeted the amyloid β (Aβ) protein; however, there has recently been increased interest in other targets including phosphorylated tau and other forms of tau. 1 key finding →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder characterized by severe motor, cognitive and psychiatric impairments. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Progressive supranuclear palsy (PSP) is a common cause of atypical parkinsonism and a rapidly progressive disease that greatly burdens both patients and caregivers. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
In 2011, a hexanucleotide repeat expansion in the first intron of the C9orf72 gene was identified as the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is still a major public health challenge without an effective treatment to prevent or stop it. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is histopathologically characterized by aggregation of two proteins, namely amyloid-beta peptide and tau protein. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
With an ageing global population, the number of people with dementia, and its main cause Alzheimer's disease (AD), is growing. current licensed treatments available for ad are only alleviate the symptoms of the disease, and are effective only in some people with ad for a limited time. there are currently no therapies that target the disease process. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by the coexistence of amyloid-β (Aβ) plaques and tau-based neurofibrillary tangles. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
LMTM given alone increased hippocampal Acetylcholine (ACh) levels, glutamate release from synaptosomal preparations, synaptophysin levels in multiple brain regions and mitochondrial complex IV activity, reduced tau pathology, partially restored ChAT immunoreactivity in the basal forebrain and reversed deficits in spatial learning. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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 →