Exposure to ambient air pollution is a serious and common public health concern associated with growing morbidity and mortality worldwide. 4 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.
The data support that the midbrain may be more sensitive to the neuroinflammatory effects of subchronic air pollution exposure. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
40/100
The concept of the inflammasome, a macromolecular complex sensing cell stress or danger signals and initiating inflammation, was first introduced approximately a decade ago. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's dis ease (AD) is a leading cause of mortality in the developed world with 70% risk attributable to genetics. 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 affecting millions of people worldwide and will continue to affect millions more with population aging on the rise. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our results indicate that different brain regions may be uniquely responsive to changes induced by exposure to DEE. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Particulate matter with a diameter of less than 2.5 μm or PM2.5 is recognized worldwide as a cause of public health problems, mainly associated with respiratory and cardiovascular diseases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
In humans, olfactory dose of inhaled nanoparticles is highest for 1-2 nm particles with ∼1% of inhaled particles depositing in the olfactory region. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
40/100
Neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), Amyotrophic lateral sclerosis (ALS) and retinal degeneration have been studied extensively and varying molecular mechanisms have been proposed for onset of such diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Chronic exposure to particulate matter air pollution is known to cause inflammation leading to respiratory- and cardiovascular-related sickness and death. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Parkinson's disease, as well as other neurodegenerative disorders, are primarily characterized by pathological accumulation of proteins, inflammation, and neuron loss. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Exposure to air pollutants is associated with an increased risk of developing Alzheimer's disease (AD). 4 key findings →
Participants: 13 Evidence: low
Full summary, score breakdown and related studies → Original source
Decreased olfactory function is very common in the older population, being present in over half of those between the ages of 65 and 80 years and in over three quarters of those over the age of 80 years. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Pericytes are vascular mural cells embedded in the basement membrane of blood microvessels. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Glycogen synthase kinase 3 (GSK3) is a constitutively active, proline-directed serine/threonine kinase that plays a part in a number of physiological processes ranging from glycogen metabolism to gene transcription. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microglia make up the innate immune system of the central nervous system and are key cellular mediators of neuroinflammatory processes. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The pro-inflammatory activation of microglia is a hallmark of Alzheimer's disease (AD), and this process involves a switch from oxidative phosphorylation (OXPHOS) toward glycolysis. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The role of tumor necrosis factor (TNF) as an immune mediator has long been appreciated but its function in the brain is still unclear. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
We present the preliminary neuropathologic criteria for progressive supranuclear palsy (PSP) as proposed at a workshop held at the National Institutes of Health, Bethesda, MD, April 24 and 25, 1993. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The neurone-centred view of the past disregarded or downplayed the role of astroglia as a primary component in the pathogenesis of neurological diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Severe amyloidosis and plaque-localized neuro-inflammation are key pathological features of Alzheimer's disease (AD). 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
These findings support that a complex gut microbiome is required for behavioural defects, microglia activation and AD pathologies, the gut microbiome contributes to pathologies in an AD mouse model and that dysbiosis of the human microbiome might be a risk factor for AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The gut microbiota is a complex ecosystem that comprises of more than 100 trillion symbiotic microbial cells. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
An excess of saturated fatty acids and simple sugars in the diet is a known environmental risk factor of Alzheimer's disease (AD) but the holistic view of the interacting processes through which such diet may contribute to AD pathogenesis is missing. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The human microbiome consists of ~3.8 × 10 13 symbiotic microorganisms that form a highly complex and dynamic ecosystem: the gastrointestinal (GI) tract constitutes the largest repository of the human microbiome by far, and its impact on human neurological health and disease is becoming increasingly appreciated. 5 key findings →
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.
- Comprehensive Evaluation of the 5XFAD Mouse Model for Preclinical Testing Applications: A MODEL-AD Study
- Amyloid beta-peptide (1-42)-induced oxidative stress and neurotoxicity: implications for neurodegeneration in Alzheimer's disease brain. A review
- PSEN1ΔE9, APPswe, and APOE4 Confer Disparate Phenotypes in Human iPSC-Derived Microglia
- A Review of Recent Advances in the Management of Alzheimer's Disease
- Blood cadmium levels and Alzheimer's disease mortality risk in older US adults
- The potent BACE1 inhibitor LY2886721 elicits robust central Aβ pharmacodynamic responses in mice, dogs, and humans
- Cerebrospinal fluid tau and beta-amyloid(1-42) in dementia disorders
- Tangle and neuron numbers, but not amyloid load, predict cognitive status in Alzheimer's disease
- Pathological roles of MAPK signaling pathways in human diseases
- Avanços na doença de Alzheimer: diagnóstico precoce, biomarcadores e perspectivas futuras
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 →