Alzheimer's disease (AD) patients often have visual disorders which may be due to retinal nerve degenerative changes. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
30,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Non-motor manifestations of Parkinson disease (PD) are common and some may actually antedate motor dysfunction. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Extracellular adenosine 5'-triphosphate (ATP) has been recognized as a ubiquitous, unstable signalling molecule, acting as a fast neurotransmitter and modulator of transmitter release and neuronal excitability. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The discovery in 1997 that mutations in the SNCA gene cause Parkinson's disease (PD) greatly advanced our understanding of this illness. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
In contrast to other tissues, the nervous system is enriched in the polyunsaturated fatty acids (PUFAs): arachidonic acid (AA, 20:4 n-6) and docosahexaenoic acid (DHA, 22:6 n-3). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Docosahexaenoic acid (DHA, 22:6n-3) and arachidonic acid (AA, 20:4n-6) are the major polyunsaturated fatty acids in the membranes of brain and retinal cells. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent findings The docosahexaenoate-derived mediator neuroprotectin D1 is formed in retinal pigment epithelial cells when confronted with oxidative stress, in the brain during experimental stroke, and in the human brain from Alzheimer's disease patients as well as in human brain cells in culture. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Parkinson's disease is characterized by a slowing of resting state brain activity involving theta, beta and gamma frequency bands. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The authors have devised, implemented, and tested a fast, spatially accurate technique for calculating the high-dimensional deformation field relating the brain anatomies of an arbitrary pair of subjects. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Increasing evidence indicates that hyperglycemia is the initiating cause of the tissue damage occurring in diabetes, either through repeated acute changes in cellular glucose metabolism, or through the long-term accumulation of glycated biomolecules and advanced glycation end products (AGEs). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alpha-linolenic acid (18:3omega3) deficiency alters the structure and function of membranes and induces minor cerebral dysfunctions, as demonstrated in animal models and subsequently in human infants. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
36/100
CONSIDERABLE interest has been focused on the entity of progressive external ophthalmoplegia (PEO) since the report of Kiloh and Nevin in 1951.1These authors were primarily concerned with the pathogenesis of the ocular muscle weakness, concluding that it was virtually always the result of a myopathic process. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia manifested by vivid, often frightening dreams associated with simple or complex motor behavior during REM sleep. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Compared with the normal controls, PTSD patients showed increased local coherence in subcortical regions, including amygdala, hippocampus, thalamus, and putamen, and decreased local coherence in cortical regions, including medial prefrontal cortex and dorsolateral prefrontal cortex. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Primary pathologies including amyloid-β (Aβ) plaques and neurofibrillary tangles (NFT) develop many years before the onset of dementia symptoms in Alzheimer's disease (AD). 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The presence of neurofibrillary tangles in the brain is a hallmark feature of several neurodegenerative diseases termed "tauopathies," including Alzheimer's disease (AD) and the tau molecular subgroup of frontotemporal lobar degeneration (FTLD-tau). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Abnormal accumulation of tau aggregates in the brain is one of the hallmarks of Alzheimer disease neuropathology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Inverse correlations between amyloid-beta (Abeta) load measured by Pittsburgh Compound-B (PiB) positron emission tomography (PET) and cerebral metabolism using [(18)F]fluoro-2-deoxy-d-glucose (FDG) in Alzheimer's disease (AD) patients, suggest local Abeta-induced metabolic insults. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The accumulation of amyloid-β (Aβ) plaques is a central feature of Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The lack of a specific biomarker makes preclinical diagnosis of Alzheimer's disease (AD) impossible, and it precludes assessment of therapies aimed at preventing or reversing the course of the disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Positron emission tomography (PET) of brain amyloid β is a technology that is becoming more available, but its clinical utility in medical practice requires careful definition. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
36/100
The ε4 allele of the polymorphic apolipoprotein E gene is associated with increased risk of Alzheimer's disease (AD), deposition of β-amyloid (Aβ), and reduction in cerebral glucose metabolism in asymptomatic people. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Recent studies in mouse models of Alzheimer's disease (AD) and in humans suggest that sleep disruption and amyloid-beta (Aβ) accumulation are interrelated, and may, thus, exacerbate each other. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Use of biomarkers in the detection of early and preclinical Alzheimer's disease (AD) has become of central importance following publication of the NIA-Alzheimer's Association revised criteria for the diagnosis of AD, mild cognitive impairment (MCI) and preclinical AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer disease (AD) is one of, if not the most, feared diseases associated with aging. 3 key findings →
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 30,180 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 30,180 records, built mostly from automated pulls of Europe PMC (64.2% of the library) and OpenAlex (16.9%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 →