Probiotic supplements were shown to improve cognitive function in Alzheimer's disease (AD) patients. 2 key findings →
Participants: 21 Evidence: low
Full summary, score breakdown and related studies → Original source
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Probiotic supplements were shown to improve cognitive function in Alzheimer's disease (AD) patients. 2 key findings →
Participants: 21 Evidence: low
Full summary, score breakdown and related studies → Original source
The evolution of the understanding of the intestinal microbiota and its influence on our organism leverages it as a potential protagonist in therapies aimed at diseases that affect not only the intestine but also neural pathways and the central nervous system itself. 5 key findings →
Design: systematic review Evidence: high
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) pathology is thought to progress from normal cognition through preclinical disease and ultimately to symptomatic AD with cognitive impairment. 3 key findings →
Design: cross-sectional Participants: 164 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The loss of excitatory synapses is known to underlie the cognitive deficits in Alzheimer's disease (AD). 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD), is a chronic age-related progressive neurodegenerative disorder, characterized by neuroinflammation and extracellular aggregation of Aβ peptide. 3 key findings →
Participants: 14 Evidence: low
Full summary, score breakdown and related studies → Original source
Vascular mechanisms of Alzheimer's disease (AD) may constitute a therapeutically addressable biological pathway underlying dementia. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease is a complex neurodegenerative disorder leading to a decline in cognitive function and mental health. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tauopathies are a diverse group of progressive and fatal neurodegenerative diseases characterized by aberrant tau inclusions in the central nervous system. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Tau-mediated neurodegeneration is a hallmark of Alzheimer's disease. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Clinical and animal studies have shown that gut microbiome disturbances can affect neural function and behaviors via the microbiota-gut-brain axis, and may be implicated in the pathogenesis of several brain diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by amyloid-β accumulation in the brain and hyperphosphorylated tau aggregation, as well as neuroinflammation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease, the most common cause of dementia, is a chronic degenerative disease with typical pathological features of extracellular senile plaques and intracellular neurofibrillary tangles and a significant decrease in the density of neuronal dendritic spines. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The blood-brain barrier (BBB) is a unique and selective feature of the central nervous system's vasculature. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a brain disorder that progressively undermines memory and thinking skills by affecting the hippocampus and entorhinal cortex. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is one of the most common neurodegenerative disorders associated with age or inherited mutations. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The accumulated evidence on increased levels of inflammatory markers in the cerebrospinal fluid (CSF) of AD patients, along with reports describing CNS alterations caused by senescent immune cells in neuro-degenerative diseases, set out a conceptual framework in which the neuroinflammation hypothesis is being challenged from different angles towards developing new therapies against AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mitochondria play a key role in both health and disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The gut microbiota (GM) plays an important role in the physiology and pathology of the host. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Inflammatory Bowel Disease (IBD), a chronic nonspecific intestinal inflammatory disease, is comprised of Ulcerative Colitis (UC) and Crohn's Disease (CD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
JOURNAL/nrgr/04.03/01300535-202410000-00029/figure1/v/2024-02-06T055622Z/r/image-tiff Disturbances in the microbiota-gut-brain axis may contribute to the development of Alzheimer's disease. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Disturbances in the local and peripheral immune systems are closely linked to a wide range of diseases. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
We have recently shown that multiple tRNA synthetase inhibitors can greatly increase lifespan in multiple models by acting through the conserved transcription factor ATF4. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Our understanding of stress granule (SG) biology has deepened considerably in recent years, and with this, increased understanding of links has been made between SGs and numerous neurodegenerative diseases. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Intraneuronal dysproteostasis and extraneuronal microenvironmental abnormalities in Alzheimer's disease (AD) collectively culminate in neuronal deterioration. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The advent of high-throughput 'omics' technologies has improved our knowledge of gut microbiome in human health and disease, including Alzheimer's disease (AD), a neurodegenerative disorder. 5 key findings →
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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.
1,032 records (3.8% 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 →