3 Science-Backed Ways To Support Memory & Brain Health With Diet by mindbodygreen

 Don't let your incompetent? doctor give you guidelines like this! You need SPECIFICS, like an EXACT DIET PROTOCOL! 

3 Science-Backed Ways To Support Memory & Brain Health With Diet

Safety and efficacy of faecal microbiota transplantation in patients with mild to moderate Parkinson's disease (GUT-PARFECT): a double-blind, placebo-controlled, randomised, phase 2 trial

 

With your risk of Parkinsons post stroke, your competent? doctor and hospital should be ensuring that they know which intervention is better for Parkinsons. Or don't you have a competent doctor or hospital?

 This one or the newest one?Trial of Lixisenatide in Early Parkinson’s Disease April 2024

 

Do you prefer your  doctor and hospital incompetence NOT KNOWING? OR NOT DOING?

Parkinson’s Disease May Have Link to Stroke March 2017

The latest here:

Safety and efficacy of faecal microbiota transplantation in patients with mild to moderate Parkinson's disease (GUT-PARFECT): a double-blind, placebo-controlled, randomised, phase 2 trial

• Arnout Bruggeman
• Charysse Vandendriessche
• Hannelore Hamerlinck
• Danny De Looze
• David J. Tate
• Marnik Vuylsteke
• et al.
• Show all authors
• Show footnotes

Open AccessPublished:March 27, 2024DOI:https://doi.org/10.1016/j.eclinm.2024.102563

Summary

Background

Dysregulation of the gut microbiome has been implicated in Parkinson's disease (PD). This study aimed to evaluate the clinical effects and safety of a single faecal microbiota transplantation (FMT) in patients with early-stage PD.

Methods

The GUT-PARFECT trial, a single-centre randomised, double-blind, placebo-controlled trial was conducted at Ghent University Hospital between December 01, 2020 and December 12, 2022. Participants (aged 50–65 years, Hoehn and Yahr stage 2) were randomly assigned to receive nasojejunal FMT with either healthy donor stool or their own stool. Computer-generated randomisation was done in a 1:1 ratio through permutated-block scheduling. Treatment allocation was concealed for participants and investigators. The primary outcome measure at 12 months was the change in the Movement Disorders Society-Unified Parkinson's Disease Rating Scale (MDS-UPDRS) motor score obtained during off-medication evaluations. Intention-to-treat analysis was performed using a mixed model for repeated measures analysis. This completed trial is registered on ClinicalTrials.gov (NCT03808389).

Findings

Between December 2020 and December 2021, FMT procedures were conducted on 46 patients with PD: 22 in the healthy donor group and 24 in the placebo group. Clinical evaluations were performed at baseline, 3, 6, and 12 months post-FMT. Full data analysis was possible for 21 participants in the healthy donor group and 22 in the placebo group. After 12 months, the MDS-UPDRS motor score significantly improved by a mean of 5.8 points (95% CI −11.4 to −0.2) in the healthy donor group and by 2.7 points (−8.3 to 2.9) in the placebo group (p = 0.0235). Adverse events were limited to temporary abdominal discomfort.

Interpretation

Our findings suggested a single FMT induced mild, but long-lasting beneficial effects on motor symptoms in patients with early-stage PD. These findings highlight the potential of modulating the gut microbiome as a therapeutic approach and warrant a further exploration of FMT in larger cohorts of patients with PD in various disease stages.

Funding

Flemish PD patient organizations (VPL and Parkili), Research Foundation Flanders (FWO), Biocodex Microbiota Foundation.

Keywords

• Parkinson's disease
• Gut-brain axis
• Faecal microbiota transplantation
• Clinical trial
• Gut microbiota

Research in context

Evidence before this study

A comprehensive search was conducted on PubMed from database inception till September 1st, 2023, using the search terms “Parkinson” and “gut microbiota” or “gut microbiome”, without any language or date restrictions. The existing literature supports an early involvement of the gastrointestinal system in the aetiology and progression of Parkinson's disease (PD) for a sub-group of patients, supporting the gut-first versus brain-first hypothesis. During the prodromal phase of the disease, evidence suggests the presence of alpha-synuclein in the enteric nervous system, subclinical gut inflammation, compromised intestinal barrier integrity, and gastrointestinal symptoms like constipation. Several recent meta-analyses comparing the gut microbiota of patients with PD to healthy controls have shown differential abundances of taxa associated with reduced mucosal barrier and increased intestinal inflammation. An additional search was performed on PubMed using the terms “Parkinson” and “microbiota transplantation” which yielded 82 reports predominantly focusing on faecal microbiota transplantation (FMT) as a potential treatment for PD. Four open-label studies with small number of patients have demonstrated beneficial effects on symptoms, mainly constipation. Although technically not a FMT study, a recently conducted pilot study with a randomized and placebo-controlled design (n = 11), using an orally lyophilised donor stool product or matching placebo, was well tolerated and reported reduced constipation, however objective UPDRS motor improvements were transient and not statistically different from placebo. In these studies, adverse events associated with FMT were mild and restricted to transient gastro-intestinal discomfort and diarrhoea.

Added value of this study

We present the results of a one-year, randomized, double-blind, placebo-controlled study of nasojejunal FMT in patients with early-stage PD. This study is the first of its kind with larger sample sizes compared to previously reported trials. The healthy donor FMT group demonstrated significantly greater improvements in motor symptom severity compared to the control group, with the effect becoming more pronounced starting from the 6 to 12 months interval. Objective measurements of gastrointestinal transit indicated improvements in the healthy donor group, starting from the 3 to 6 months interval. No severe adverse events were reported in either group, further supporting the safety profile of FMT.

 

More at link.

Alzheimer’s Symptoms Transferred via Microbiota Transplant

I can't tell if this includes fecal transplants or not. But beware.

Alzheimer’s Symptoms Transferred via Microbiota Transplant

Summary: A new study confirmed a link between gut microbiota and Alzheimer’s disease.

The research demonstrated that Alzheimer’s symptoms could be transferred to young, healthy organisms through gut microbiota transplants. Alzheimer’s patients exhibited a heightened presence of inflammation-causing bacteria, correlating with their cognitive state.

This discovery emphasizes the gut microbiome as a pivotal area of investigation for Alzheimer’s.

Key Facts:

1. Memory impairments in Alzheimer’s patients can be transferred to young animals via gut microbiota transplants.
2. Increased inflammation-promoting bacteria in the gut is directly connected to cognitive decline in Alzheimer’s patients.
3. The research suggests that early intervention by studying the role of gut microbes during the initial stages of dementia could lead to new therapeutic approaches.

Source: UCC

Researchers have discovered the link between the gut microbiota and Alzheimer’s disease.

For the first time, researchers have found that Alzheimer’s symptoms can be transferred to a healthy young organism via the gut microbiota, confirming its role in the disease.

The research was led by Professor Yvonne Nolan, APC Microbiome Ireland, a world leading SFI funded research centre based at University College Cork (UCC), and the Department of Anatomy and Neuroscience, UCC, with Professor Sandrine Thuret at King’s College London and Dr Annamaria Cattaneo IRCCS Fatebenefratelli, Italy.

The study supports the emergence of the gut microbiome as a key target for investigation in Alzheimer’s disease due to its particular susceptibility to lifestyle and environmental influences.

Published in Brain, the study shows that that the memory impairments in people with Alzheimer’s could be transferred to young animals through transplant of gut microbiota.

Alzheimer’s patients had a higher abundance of inflammation-promoting bacteria in faecal samples, and these changes were directly associated with their cognitive status.

Professor Yvonne Nolan said: “The memory tests we investigated rely on the growth of new nerve cells in the hippocampus region of the brain. We saw that animals with gut bacteria from people with Alzheimer’s produced fewer new nerve cells and had impaired memory.”

“People with Alzheimer’s are typically diagnosed at or after the onset of cognitive symptoms, which may be too late, at least for current therapeutic approaches. Understanding the role of gut microbes during prodromal – or early stage- dementia, before the potential onset of symptoms may open avenues for new therapy development, or even individualised intervention,” said Professor Nolan.

Alzheimer’s is the most common cause of dementia, a general term for memory loss and other cognitive abilities serious enough to interfere with daily life. As our population ages, one in three people born today are likely to develop Alzheimer’s.

Funded by Science Foundation Ireland, scientists in UCC are working to develop strategies to promote healthy brain ageing and advance treatments for Alzheimer’s by exploring how the gut microbiota respond to lifestyle influences like diet and exercise.

Professor Sandrine Thuret, Professor of Neuroscience at King’s College London and one of the study’s senior authors said, “Alzheimer’s is an insidious condition that there is yet no effective treatment for. This study represents an important step forward in our understanding of the disease, confirming that the make-up of our gut microbiota has a causal role in the development of the disease.

“This collaborative research has laid the groundwork for future research into this area, and my hope is that it will lead to potential advances in therapeutic interventions.”

The research was conducted by Dr Stefanie Grabrucker, a postdoctoral researcher working with Professor Nolan, in partnership with postdoctoral colleagues Dr Edina Silajdzic at King’s College London and Dr Moira Marizzoni, IRCCS Fatebenefratelli, Italy. UCC collaborators were Professor Cora O’Neill, Dr Olivia O’Leary, Dr Sarah Nicolas, Dr Jane English, Mr Sebastian Dohm-Hansen and Dr Aonghus Lavelle.

Professor. John F. Cryan, UCC Vice President for Research and Innovation, who was also involved in this research said: “I’m delighted to be involved in this exciting study that further enhances our understanding of the significant role played by the gut microbiome in brain related diseases, such as Alzheimer’s, and recognises UCC and APC Microbiome Ireland as leading institutions in microbiome and brain health research.

“This research aligns with our UCC Futures Framework and the strategic plan for the University in the areas of Food, Microbiome and Health and the soon to be launched Future Ageing and Brain Science.”

About this Alzheimer’s disease research news

Author: Kate O Sullivan
Source: UCC
Contact: Kate O Sullivan – UCC
Image: The image is credited to Neuroscience News

Original Research: Open access.
“Microbiota from Alzheimer’s patients induce deficits in cognition and hippocampal neurogenesis” by Yvonne Nolan et al. Brain

Human umbilical cord plasma proteins revitalize hippocampal function in aged mice

But is cannabis, young blood, young gut bacteria or poo transplants better? You do expect your doctor to know this answer? Don't you? Or are you acknowledging that your doctor doesn't keep up with research and thus knows nothing about how to get you 100% recovered? A binary question. Knows the answer or is not a doctor at all.

Cannabis Reverses Aging Processes in the Brain

Can we reverse the ageing process by putting young blood into older people?

Restoring gut bacteria to youthful age linked to improved stroke recovery in mice

Poo transplants better understood

 

 

 

https://www.nature.com/articles/nature22067

• Joseph M. Castellano
• , Kira I. Mosher
• , Rachelle J. Abbey
• , Alisha A. McBride
• , Michelle L. James
• , Daniela Berdnik
• , Jadon C. Shen
• , Bende Zou
• , Xinmin S. Xie
• , Martha Tingle
• , Izumi V. Hinkson
• , Martin S. Angst
•  & Tony Wyss-Coray

• Nature 544, 488–492 (27 April 2017)
• doi:10.1038/nature22067
• Download Citation
• • Blood–brain barrier
  • Hippocampus
  • Learning and memory
  • Neural circuits
  • Neuroimmunology

Received:

19 November 2015

Accepted:

14 March 2017

Published online:

19 April 2017

Abstract

Ageing drives changes in neuronal and cognitive function, the decline of which is a major feature of many neurological disorders. The hippocampus, a brain region subserving roles of spatial and episodic memory and learning, is sensitive to the detrimental effects of ageing at morphological and molecular levels. With advancing age, synapses in various hippocampal subfields exhibit impaired long-term potentiation¹, an electrophysiological correlate of learning and memory. At the molecular level, immediate early genes are among the synaptic plasticity genes that are both induced by long-term potentiation^2,3,4 and downregulated in the aged brain^5,6,7,8. In addition to revitalizing other aged tissues^{9,10,11,12,13}, exposure to factors in young blood counteracts age-related changes in these central nervous system parameters^14,15,16, although the identities of specific cognition-promoting factors or whether such activity exists in human plasma remains unknown¹⁷. We hypothesized that plasma of an early developmental stage, namely umbilical cord plasma, provides a reservoir of such plasticity-promoting proteins. Here we show that human cord plasma treatment revitalizes the hippocampus and improves cognitive function in aged mice. Tissue inhibitor of metalloproteinases 2 (TIMP2), a blood-borne factor enriched in human cord plasma, young mouse plasma, and young mouse hippocampi, appears in the brain after systemic administration and increases synaptic plasticity and hippocampal-dependent cognition in aged mice. Depletion experiments in aged mice revealed TIMP2 to be necessary for the cognitive benefits conferred by cord plasma. We find that systemic pools of TIMP2 are necessary for spatial memory in young mice, while treatment of brain slices with TIMP2 antibody prevents long-term potentiation, arguing for previously unknown roles for TIMP2 in normal hippocampal function. Our findings reveal that human cord plasma contains plasticity-enhancing proteins of high translational value for targeting ageing- or disease-associated hippocampal dysfunction.

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Poo transplants better understood

Since you might be a candidate for this your doctor needs to understand this more fully. Do you trust your doctor to be up-to-date on research? I wouldn't.

Restoring gut bacteria to youthful age linked to improved stroke recovery in mice

Transfer of gut bacteria affects brain function and nerve fiber insulation

Poo transplants better understood

27 April 2016 European Molecular Biology Laboratory (EMBL)

• Under embargo until 28 April 2016 18:00 GMT

For the first time, scientists studying stool transplants have been able to track which strains of bacteria from a donor take hold in a patient’s gut after a transplant. The team, led by EMBL with collaborators at Wageningen University and the Academic Medical Centre, both in the Netherlands, and the University of Helsinki, Finland found that compatibility between donor and patient likely plays a bigger role in these transplants than previously thought. The study, published today in Science, could help make stool transplants a valid treatment option for more conditions than they are currently applied to.
“Ultimately, the goal is to move from a stool transplant to something more manageable, such as a pill,” says Simone Li, who carried out the work at EMBL. “Our work shows that this is likely going to be a personalised bacterial cocktail, rather than a one-size-fits-all solution.”
Stool transplants – also known as faecal microbiota transplants – involve taking microbes from the poo of a healthy donor and transferring them to the patient’s gut. The hope is that this will help to restore health to patients suffering from conditions where the normal balance of microbes in the gut gets skewed. The approach has been very successful for treating recurrent Clostridium difficile (C. diff) infections – which can cause life-threatening cases of diarrhoea, and are becoming a serious problem in hospitals and healthcare institutes. But for other conditions, like ulcerative colitis, stool transplants have proven much less effective. The current study, led by Peer Bork and Shinichi Sunagawa at EMBL, could help improve those odds. The trick, the scientists say, is to look beyond what species of microbes are in a person’s gut, to what strains of each species.
Most people have E. coli in their gut, for instance, but different people have different strains of this species – and some of those strains can cause health issues. By distinguishing between different strains, the EMBL scientists were able to track if the microbes in a patient’s gut after the treatment were their own or came from the donor.
They found that after a stool transplant, new strains of microbes from the donor were more likely to colonise a patient’s gut if the patient already had that species. This implies that if doctors can match donors to patients, the chances of the treatment being a success could improve considerably. Looking at strains rather than species of bacteria could also make the therapy effective in conditions where it isn’t currently working.
“With this method, we can really see if, for example, an antibiotic-resistant strain is replaced by a non-resistant one,” says microbiologist Willem de Vos, who led the work at Wageningen University and the University of Helsinki, “so it could help to design stool transplants to work in other conditions beyond C. diff.”
The study builds on a clinical trial that looked into the use of stool transplants as a treatment for metabolic syndrome, run by Max Nieuwdorp at the Academic Medical Centre in Amsterdam. Although based on data from only 10 people, the work already provides strong indications that donor-patient compatibility is more important than assumed: transplants from one donor led to very different outcomes in three different patients.
http://s.embl.org/pr280416

• Full bibliographic informationLi SS et al. Durable coexistence of donor and recipient strains after fecal microbiota transplantation. Science, 28 April 2016.

Transfer of gut bacteria affects brain function and nerve fiber insulation

So maybe you want a fecal transplant from a happy person to treat your depression. I'm assuming that this would work the same way in reverse as this research shows. 

Transfer of gut bacteria affects brain function and nerve fiber insulation

The Mount Sinai Hospital, 04/22/2016

Specific combinations of gut bacteria produce substances that affect myelin content and cause social avoidance behaviors in mice, according to a study conducted at the Icahn School of Medicine at Mount Sinai and published in the journal eLife. This research suggests that targeting intestinal bacteria, or their metabolites, could be one way to treat debilitating psychiatric disorders and demyelinating diseases, like multiple sclerosis. This current study led by Patrizia Casaccia, MD, PhD, Professor of Neuroscience, Genetics and Genomics, and Neurology, and Chief of the Center of Excellence for Myelin Repair, and post–doctoral fellow Mar Gacias, PhD, identifies bacteria–derived gut metabolites that can affect myelin content in the brains of mice and induce depression–like symptoms. Researchers transferred fecal bacteria from the gut of depressed mice to genetically distinct mice exhibiting non–depressed behavior. The study showed that the transfer of microbiota was sufficient to induce social withdrawal behaviors and change the expression of myelin genes and myelin content in the brains of the recipient mice. In an effort to define the mechanism of gut–brain communication, researchers identified bacterial communities associated with increased levels of cresol, a substance that has the ability to pass the blood–brain barrier. When the precursors of myelin–forming cells were cultured in a dish and exposed to cresol, they lost their ability to form myelin, thereby suggesting that a gut–derived metabolite impacted myelin formation in the brain.