27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
Oral treatment of the amyloid prone AD-like APPPS1 mice with spermidine reduced neurotoxic soluble Aβ and decreased AD-associated neuroinflammation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Pg OMVs impaired memory and learning ability of mice and decreased tight junction-related gene expression ZO-1, occludin, claudin-5, and occludin protein expression in the hippocampus. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common cause of dementia in the general population and, to date, constitutes a major therapeutic challenge. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Extensive human studies and animal models show that chronic immune system stimulation involving microglia, inflammasome, complement activation, synthesis of cytokines, and reactive oxygen species exacerbates neurodegeneration in Alzheimer's disease (AD) and other tauopathies. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
There is an increasing prevalence of Vascular Cognitive Impairment (VCI) worldwide, and several studies have suggested that Chronic Cerebral Hypoperfusion (CCH) plays a critical role in disease onset and progression. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most common form of dementia among several neurodegenerative disorders afflicting the elderly. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuroinflammation is the fundamental immune response against multiple factors in the central nervous system and is characterized by the production of inflammatory mediators, activated microglia and astrocytes, and the recruitment of innate and adaptive immune cells to inflammatory sites, that contributes to the pathological process of related brain diseases, such as Alzheimer's disease, Parkinson's disease, depression, and stroke. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Inflammasomes are intracellular protein complexes, members of the innate immune system, and their activation and regulation play an essential role in maintaining homeostatic conditions against exogenous and endogenous stimuli. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
The pathogenesis of neurodegenerative diseases involves the accumulation of misfolded protein aggregates. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A growing body of basic research has shown that EA can ameliorate neuroinflammation centrally (in animal models of ischemic stroke, Alzheimer's disease, traumatic brain injury, spinal cord injury, Parkinson's disease and vascular dementia) and peripherally (e.g. after a surgical insult or injection of lipopolysaccharide) and that its effects involve different molecular mechanisms, including activation of the α7 nicotinic acetylcholine receptor signaling pathway and P2 type purinergic receptors, inhibition of nuclear factor κB, and mitigation of damage secondary to oxidative stress and NOD-like receptor protein 3 inflammasome activation. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Autophagy degrades phagocytosed damaged organelles, misfolded proteins, and various pathogens through lysosomes as an essential way to maintain cellular homeostasis. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Neuroinflammation is considered one of major factors in the pathogenesis of Alzheimer's disease (AD). 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The oral cavity is the initial chamber of digestive tract; the saliva swallowed daily contains an estimated 1.5 × 1012 oral bacteria. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The gut-brain axis describes a bidirectional interplay within the enteric environment between the intestinal epithelium, the mucosal immune system, and the microbiota with the enteric nervous system. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
An epidemic of age-associated cognitive decline, most commonly ascribed to neurodegenerative conditions such as Alzheimer's and Parkinson's disease, is causing healthcare costs to soar and devastating caregivers. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Initial studies suggested that the fluctuations in the quantity, variety, and composition of the gut microbiota can significantly affect disease processes. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Evidence that the gut microbiota plays a key role in the pathogenesis of Alzheimer's disease is already unravelling. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Microbial-derived metabolites are the intermediate or end products of bacterial digestion. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) and related dementias (ADRD) are still a serious global public health concern more than a century after the German neuropathologist and psychiatrist Dr. Aloysius Alzheimer described the first case. 5 key findings →
Design: narrative review Evidence: low
Full summary, score breakdown and related studies → Original source
Lewy body diseases, such as Parkinson's disease and dementia with Lewy bodies, vary in their clinical phenotype but exhibit the same defining pathological feature, α-synuclein aggregation. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Hundreds of billions of commensal microorganisms live in and on our bodies, most of which colonize the gut shortly after birth and stay there for the rest of our lives. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Given the complex bidirectional communication system that exists between the gut microbiome and the brain, there is growing interest in the gut microbiome as a novel and potentially modifiable risk factor for Alzheimer's disease (AD). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is the most prevalent form of dementia and can be influenced by genetic and environmental factors. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Emerging evidence suggests that both disruption of circadian rhythms and gut dysbiosis are closely related to aging-associated neurodegenerative diseases. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD), the most common neurodegenerative disorder, is accompanied by cognitive impairment and shows representative pathological features, including senile plaques and neurofibrillary tangles in the brain. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
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
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.
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.
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 →