All articles tagged with #gut brain axis
Alzheimer’s is viewed as a complex system driven by amyloid-beta and tau, aging, and systemic health; single-target drugs have limited impact, so researchers are pushing integrated, multi-pronged therapies—combining approaches like gene editing, senolytics, metabolic interventions, and gut-brain axis strategies—guided by early biomarkers and advanced models to slow, halt, or prevent disease progression.
In a 12-week, double-blind twin study from King's College London, older adults consuming a daily prebiotic blend (inulin or FOS) with protein powder showed improved memory test scores and subtle gut microbiome changes (including more Bifidobacterium) versus their co-twins taking a placebo, with no significant physical benefits observed. The findings support the gut-brain axis as a potential target for aging-related cognitive decline, though larger, longer trials are needed.
UC San Francisco researchers reveal a two-stage gut signaling pathway: parasite detection by tuft cells releases acetylcholine, which prompts enterochromaffin cells to release serotonin and activate vagal brain signals, leading to delayed appetite suppression as infection takes hold; the finding links gut immune response to behavior and could inform gut disorders like IBS and food intolerances.
New research reveals a two-phase, paracrine dialogue between gut tuft cells and serotonergic enterochromaffin (EC) cells that links parasite detection to brain signaling and feeding behavior. Tuft cells release acetylcholine (ACh) in an acute, parasite-triggered fashion and also a constitutive leak during type 2 inflammation; both modes can activate EC cells, but only sustained ACh release raises serotonin enough to stimulate vagal afferents and suppress food intake. This epithelial crosstalk couples type 2 immune responses with sensory signaling to drive gut–brain communication and protective behaviors during parasitic infections, explaining progression from asymptomatic to symptomatic disease.
A new Science China Life Sciences review argues that Alzheimer’s arises from a complex network of factors—amyloid and Tau pathology, genetics, aging, and systemic health—making single-target drugs insufficient. The authors urge a holistic strategy that tackles multiple disease pathways, including Tau and aging-related changes, genetic risk, and gut-brain interactions, while leveraging tools like iPSC-derived organoids, CRISPR, and early biomarkers (e.g., plasma pTau217) to guide precision therapies and possibly delay or prevent progression.
Emory researchers in mouse models of leaky gut and disease show very small numbers of live gut bacteria can reach the brain, with evidence that the vagus nerve serves as the main route; blocking the nerve reduced brain bacterial presence, suggesting a gut-to-brain transmission axis influenced by diet and genetics and potentially reversible by restoring gut integrity. The findings, published in PLOS Biology, are not yet known to occur in humans and the bacteria were present in very low amounts, leaving open questions about their role in inflammation or disease and whether future gut-targeted therapies could affect brain conditions.
A review of 15 trials with about 4,275 adults suggests that modulating the gut microbiome through diet, probiotics/prebiotics, or fecal microbiota transplantation can modestly improve memory, executive function, and overall cognition in older adults—especially those with early cognitive impairment—though effects are limited in advanced Alzheimer's. Dietary approaches like the Mediterranean diet show promise, FMT shows rapid microbial shifts with some cognitive gains in small Alzheimer’s cases, but long-term safety and efficacy require more randomized trials.
In a two-year study of 656 older adults with metabolic syndrome, those who used virgin olive oil showed better cognitive performance and greater gut microbiome diversity than those using refined olive oil, likely due to polyphenols; findings are associative, not causative, and more research is needed to understand mechanisms and long-term effects.
A study from Emory University in mice shows that a high-fat Western-style diet increases gut permeability, allowing live gut bacteria to travel through the vagus nerve into the brain, which could help explain links between diet and neurological conditions; the movement was tracked using an engineered barcoded bacterium, occurred without bacteria appearing in the blood, and returning to a normal diet reduced brain bacterial load, suggesting reversibility.
Case Western Reserve University researchers report a gut-brain connection in ALS and frontotemporal dementia (FTD): harmful gut bacteria may produce inflammatory glycogen-like sugars that trigger immune responses damaging brain cells. In a study of 23 ALS/FTD patients, about 70% had high levels of these sugars versus roughly 33% of controls, suggesting gut microbes could act as an environmental trigger, especially in C9orf72 mutation carriers. The work identifies potential biomarkers and gut-targeted therapies, including degrading the sugars and modulating gut-brain signaling, with germ-free mouse models and a novel sterile housing system enabling larger-scale studies; preliminary results hint that reducing these sugars could improve brain health and may lead to clinical trials within a year.
A new review says berberine isn’t a universal metabolic fix or a hormone-like drug; it mostly acts in the gut by shaping microbiota, inflammation, and the intestinal barrier, with effects that vary by individual gut ecosystems. Its low bioavailability keeps activity local to the intestine, where microbiota may convert it into active compounds. It should be used under medical supervision due to safety concerns and drug interactions, not as a replacement for prescribed meds.
In ageing mice, the bacterium Parabacteroides goldsteinii proliferates and dampens gut-brain signalling, contributing to memory decline; transferring this microbe to young mice worsens memory, while wiping out gut bacteria or targeting P. goldsteinii with phage therapy restores memory, suggesting gut-directed treatments could combat age-related cognitive decline if the mechanism also exists in humans.
Researchers show that aging gut microbiota produce higher levels of medium-chain fatty acids, triggering peripheral inflammation via GPR84 and weakening vagal gut–brain signaling. This interoceptive dysfunction impairs hippocampal memory in aged mice, with promising interventions—phage targeting of Parabacteroides, GPR84 inhibitors, or boosting vagal activity—able to restore memory.
A randomized twin trial in adults 60+ found that a daily mix of protein plus prebiotic fructooligosaccharides improved memory on a sensitive PAL test after 12 weeks, with gut microbiota shifts (notably higher Bifidobacterium). No muscle-strength gains were observed. While the findings suggest benefits for brain health and potential dementia protection, researchers caution that larger, longer trials are needed to confirm durability and daily-life impact.
GLP-1 drugs (used for diabetes and obesity) reveal that hunger is a fluctuating biological signal governed by gut hormones and digestion, not willpower alone. By prolonging the post‑meal satiety state and slowing gastric emptying, these medications can achieve about 5–8% weight loss, though effects often fade after stopping and weight can be regained. Appetite regulation emerges from a gut–brain axis involving hormones like GLP‑1 and ghrelin, influenced by activity, nutrition, circadian rhythms, and the food environment. The broader implications include shifts in how obesity is understood, as well as ongoing questions about long‑term use, access, and nutrition management alongside treatment.