41/100
Insulin deficiency or resistance can promote dementia and hallmarks of Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Research
28,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Alzheimer's disease (AD) is the most common neurodegenerative disease characterized by extracellular deposition of amyloid beta (Aβ) leading to cognitive decline. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Following acute myocardial infarction, re-establishment of coronary perfusion aggravates further injuries in the heart and remote organs including the brain as a consequence of ischemia/reperfusion (I/R) injury. 1 key finding →
Participants: 30 Evidence: low
Full summary, score breakdown and related studies → Original source
Down syndrome (DS) is caused by trisomy of chromosome 21, which leads to a propensity to develop amyloid β (Aβ) brain pathology in early adulthood followed later by cognitive and behavioral deterioration. 2 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Tauopathies are a group of neurodegenerative disorders characterized by the aggregation of the microtubule-associated protein tau. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
The multi-site ubiquitination of Tau protein found in Alzheimer's disease filaments hints at the failed attempt of neurons to remove early toxic species. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuroinflammation is an early detectable marker of mild cognitive impairment, the transition state between normal cognition and dementia. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Insomnia is defined as difficulties of initiating and maintaining sleep, early awakening and poor subjective sleep quality despite adequate opportunity and circumstances for sleep with impairment of daytime performance. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is considered to be the most typical form of dementia that provokes irreversible cognitive impairment. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
This review explores the interface between circadian timekeeping and the regulation of brain function by astrocytes. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
Presbycusis contributes to cognitive decline and Alzheimer's disease. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
Alzheimer's disease is one of the most common age-related neurodegenerative disorders. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The fructose survival hypothesis proposes that obesity and metabolic disorders may have developed from over-stimulation of an evolutionary-based biologic response (survival switch) that aims to protect animals in advance of crisis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
With rapid aging of the population worldwide, the number of people with dementia is dramatically increasing. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease and insulin resistance are prevalent in older adults. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Obesity is a global health problem with a broad set of comorbidities, such as malnutrition, metabolic syndrome, diabetes, systemic hypertension, heart failure, and kidney failure. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Post-stroke cognitive deficits and dementia Abstract. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
When growing older, many people are faced with cognitive deterioration, which may even amount to a form of dementia at some point in time. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Late-life depression (LLD) is associated with an increased risk of all-cause dementia and may involve Alzheimer's disease pathology. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In older age, frailty is a detrimental transitional status of the aging process featuring an increased susceptibility to stressors defined by a clinical reduction of homoeostatic reserves. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
41/100
The Aβ plaque load was significantly increased in the hippocampus of PM2.5-exposed APP/PS1 mice compared to their respective FA controls. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Traffic-related air pollution (TRAP) has been a common public health problem, which is associated with central nervous system dysfunction according to large-scale epidemiological studies. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neurodegenerative diseases, featured by progressive loss of structure or function of neurons, are considered incurable at present. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
There is a huge need for novel therapeutic and preventative approaches to Alzheimer's disease (AD) and neuroinflammation seems to be one of the most fascinating solutions. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 7,799 studies in this tag that have a study page, 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 10. The same 10 appear here every time.
- Voluntary Exercise Promotes Glymphatic Clearance of Amyloid Beta and Reduces the Activation of Astrocytes and Microglia in Aged Mice
- The Impact of Gender and Estrogen on Striatal Dopaminergic Neurotoxicity
- Glycoprotein 330/megalin: probable role in receptor-mediated transport of apolipoprotein J alone and in a complex with Alzheimer disease amyloid beta at the blood-brain and blood-cerebrospinal fluid barriers
- Insulin resistance, oxidative stress and mitochondrial defects in Ts65dn mice brain: A harmful synergistic path in down syndrome
- Cyanidin-3-O-Glucoside Regulates the M1/M2 Polarization of Microglia via PPARγ and Aβ42 Phagocytosis Through TREM2 in an Alzheimer's Disease Model
- Distinct proteostasis circuits cooperate in nuclear and cytoplasmic protein quality control
- Role of neuroinflammation in neurodegeneration development
- Induction of monocyte chemoattractant protein-1 in HIV-1 Tat-stimulated astrocytes and elevation in AIDS dementia
- Single-nucleus transcriptome analysis reveals dysregulation of angiogenic endothelial cells and neuroprotective glia in Alzheimer's disease
- Autophagy and mitophagy at the synapse and beyond: implications for learning, memory and neurological disorders
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 28,980 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 28,980 records, built mostly from automated pulls of Europe PMC (62.8% of the library) and OpenAlex (17.6%), 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.
1,038 records (3.6% of the library) are not peer-reviewed — 966 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 →