Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Showing posts with label diet dementia risk. Show all posts
Showing posts with label diet dementia risk. Show all posts

Saturday, May 13, 2023

Diet and Dementia: Study Uncovers Gut-Brain Link to Alzheimer’s

Your doctor has some explaining to do. Does diet matter in preventing dementia? 

Does Diet Matter? Study Questions Links Between Diet and Dementia

 Am I reading this right? Diet has almost nothing to do with dementia?

You contradicted these?

Can Certain Foods Really Stave Off Dementia? April 2022 

Enjoy Meat? Diverse Side Dishes Lower Dementia Risk May 2020 


 

The latest here: What does your doctor say?


 

Diet and Dementia: Study Uncovers Gut-Brain Link to Alzheimer’s

Summary: A new study sheds light on the potential role of diet in preventing dementia. The analysis explored the relationship between gut health and Alzheimer’s disease, uncovering a strong link between specific types of gut bacteria and the likelihood of developing dementia.

The findings highlight the significance of gut microbiota in brain health and provide insights into the underlying mechanisms of Alzheimer’s disease.

This research opens up new avenues for personalized treatments and interventions that target gut health to potentially slow down or prevent the development of dementia.

Key Facts:

  1. The study found a significant correlation between 10 specific types of gut bacteria and the likelihood of developing Alzheimer’s disease. Six of these bacteria were identified as protective, while four were identified as risk factors for the disease.
  2. Certain bacteria in the human gut can secrete acids and toxins that interact with the APOE gene, a major risk factor for Alzheimer’s disease, triggering a neuroinflammatory response that can affect brain health and immune functions.
  3. The analysis revealed that an imbalance of gut bacteria can have negative effects on the immune system and is linked to various diseases, including depression, heart disease, cancer, and Alzheimer’s disease. This highlights the importance of maintaining a healthy balance of gut microbiota for overall health and disease prevention.

Source: University of Nevada Las Vegas

Could changing your diet play a role in slowing or even preventing the development of dementia? We’re one step closer to finding out, thanks to a new UNLV study that bolsters the long-suspected link between gut health and Alzheimer’s disease.

The analysis — led by a team of researchers with the Nevada Institute of Personalized Medicine (NIPM) at UNLV and published this spring in the Nature journal Scientific Reports — examined data from dozens of past studies into the belly-brain connection. The results? There’s a strong link between particular kinds of gut bacteria and Alzheimer’s disease.

Between 500 and 1,000 species of bacteria exist in the human gut at any one time, and the amount and diversity of these microorganisms can be influenced by genetics and diet.

This shows a brain and food.
Between 500 and 1,000 species of bacteria exist in the human gut at any one time, and the amount and diversity of these microorganisms can be influenced by genetics and diet. Credit: Neuroscience News

The UNLV team’s analysis found a significant correlation between 10 specific types of gut bacteria and the likelihood of developing Alzheimer’s disease. Six categories of bacteria — Adlercreutzia, Eubacterium nodatum group, Eisenbergiella, Eubacterium fissicatena group, Gordonibacter, and Prevotella9 — were identified as protective, and four types of bacteria — Collinsella, Bacteroides, Lachnospira, and Veillonella — were identified as a risk factor for Alzheimer’s disease.

Certain bacteria in humans’ guts can secrete acids and toxins that thin and seep through the intestinal lining, interact with the APOE (a gene identified as a major risk factor for Alzheimer’s disease), and trigger a neuroinflammatory response — affecting brain health and numerous immune functions, and potentially promoting development of the neurodegenerative disorder.   

Researchers said their novel discovery of the distinct bacterial groups associated with Alzheimer’s disease provides new insights into the relationship between gut microbiota and the world’s most common form of dementia. The findings also advance scientists’ understanding of how an imbalance of that bacteria may play a role in the disorder’s development. 

“Most of the microorganisms in our intestines are considered good bacteria that promote health, but an imbalance of those bacteria can be toxic to a person’s immune system and linked to various diseases, such as depression, heart disease, cancer, and Alzheimer’s disease,” said UNLV research professor Jingchun Chen.

“The take-home message here is that your genes not only determine whether you have a risk for a disease, but they can also influence the abundance of bacteria in your gut.” 

Credit: Neuroscience News

While their analysis established overarching categories of bacteria typically associated with Alzheimer’s disease, the UNLV team said further research is needed to drill down into the specific bacterial species that influence risk or protection. 

The hope is to one day develop treatments that are customized for an individual patient and their genetic makeup, such as medications or lifestyle change.

Studies have shown that changes in gut microbiome through probiotic use and dietary adjustments can positively impact the immune system, inflammation, and even brain function. 

“With more research it would be possible to identify a genetic trajectory that could point to a gut microbiome that would be more or less prone to developing diseases such as Alzheimer’s,” said study lead author and UNLV graduate student Davis Cammann, “but we also have to remember that the gut biome is influenced by many factors including lifestyle and diet.” 

About this Alzheimer’s disease research news

Author: Keyonna Summers
Source: University of Nevada Las Vegas
Contact: Keyonna Summers – University of Nevada Las Vegas
Image: The image is credited to Neuroscience News

Original Research: Open access.
“Genetic correlations between Alzheimer’s disease and gut microbiome genera” by Jingchun Chen et al. Scientific Reports


Abstract

Genetic correlations between Alzheimer’s disease and gut microbiome genera

A growing body of evidence suggests that dysbiosis of the human gut microbiota is associated with neurodegenerative diseases like Alzheimer’s disease (AD) via neuroinflammatory processes across the microbiota-gut-brain axis.

The gut microbiota affects brain health through the secretion of toxins and short-chain fatty acids, which modulates gut permeability and numerous immune functions. Observational studies indicate that AD patients have reduced microbiome diversity, which could contribute to the pathogenesis of the disease.

Uncovering the genetic basis of microbial abundance and its effect on AD could suggest lifestyle changes that may reduce an individual’s risk for the disease.

Using the largest genome-wide association study of gut microbiota genera from the MiBioGen consortium, we used polygenic risk score (PRS) analyses with the “best-fit” model implemented in PRSice-2 and determined the genetic correlation between 119 genera and AD in a discovery sample (ADc12 case/control: 1278/1293).

To confirm the results from the discovery sample, we next repeated the PRS analysis in a replication sample (GenADA case/control: 799/778) and then performed a meta-analysis with the PRS results from both samples.

Finally, we conducted a linear regression analysis to assess the correlation between the PRSs for the significant genera and the APOE genotypes. In the discovery sample, 20 gut microbiota genera were initially identified as genetically associated with AD case/control status.

Of these 20, three genera (Eubacterium fissicatena as a protective factor, Collinsella, and Veillonella as a risk factor) were independently significant in the replication sample. Meta-analysis with discovery and replication samples confirmed that ten genera had a significant correlation with AD, four of which were significantly associated with the APOE rs429358 risk allele in a direction consistent with their protective/risk designation in AD association.

Notably, the proinflammatory genus Collinsella, identified as a risk factor for AD, was positively correlated with the APOE rs429358 risk allele in both samples. Overall, the host genetic factors influencing the abundance of ten genera are significantly associated with AD, suggesting that these genera may serve as biomarkers and targets for AD treatment and intervention.

Our results highlight that proinflammatory gut microbiota might promote AD development through interaction with APOE. Larger datasets and functional studies are required to understand their causal relationships.

Monday, November 28, 2022

Does Diet Matter? Study Questions Links Between Diet and Dementia

Interesting, ask your doctor to clarify.

Does Diet Matter? Study Questions Links Between Diet and Dementia

Diet combined with other risk-reduction strategies may show different results

A photo of a mature couple chopping vegetables in the kitchen.

Midlife dietary habits were not tied to dementia incidence over a 20-year period, a prospective study in Sweden showed.

Adhering to conventional dietary recommendations or to a modified Mediterranean diet was not linked with lower incidence of all-cause dementia, Alzheimer's disease dementia, vascular dementia, or amyloid pathology, reported Isabelle Glans, MD, of Lund University in Sweden, and colleagues.

"The study does not exclude a possible association between diet quality and subsequent development of dementia," they wrote in Neurology.

"However, the present Swedish dietary recommendations, which are in line with those in the U.K. and U.S., or according to the Mediterranean dietary pattern, could not be confirmed to be associated with prevention of dementia," the researchers added.

It's "critically important to better understand the links between diet and nutrition and dementia risk," observed Heather Snyder, PhD, vice president of medical and scientific relations at the Alzheimer's Association in Chicago, who wasn't involved with the study.

"To get there, the connections between diet and dementia risk must be examined in multiple studies across multiple populations and even multiple countries," Snyder told MedPage Today.

"These new results represent one study and should be considered in the bigger landscape of the ongoing work," she emphasized. "This is an observational study that can find an association between factors, but does not prove causation. For that, we need an intervention study. Fortunately, there are studies today that are testing dietary and nutrition-related interventions."

"Beyond that, existing data suggest that there is synergy between different risk-reduction strategies and these strategies should be considered in combination, not one at a time," Snyder pointed out. For example, the 2-year U.S. POINTER trial is evaluating whether lifestyle interventions that target multiple risk factors can benefit people with a higher risk of cognitive decline.

The Swedish study isn't the first to suggest diet and dementia are not related. "The findings are overall in line with previous long-term studies addressing this topic," noted Nils Peters, MD, of the University of Basel in Switzerland, and Benedetta Nacmias, PhD, of the University of Florence in Italy, in an accompanying editorial.

"Diet as a singular factor may not have a strong enough effect on cognition, but is more likely to be considered as one factor embedded with various others, the sum of which may influence the course of cognitive function (diet, regular exercise, vascular risk factor control, avoiding cigarette smoking, drinking alcohol in moderation, etc.)," they wrote. "Thus, diet should rather be regarded as one part of a multidomain intervention with respect to cognitive performance."

Glans and colleagues followed 28,025 people in the Swedish population-based Malmö Diet and Cancer Study who were dementia-free at baseline and who had baseline exams from 1991-1996. Mean baseline age was 58 and 61% were women.

The researchers used a 7-day food diary, a detailed food frequency questionnaire, and a 45-60 minute interview to evaluate dietary habits at baseline.

Swedish dietary guidelines scores, designed to reflect a healthy diet based on Swedish nutritional guidelines, were calculated based on average daily food intake. Eating patterns also were assessed by adherence to a modified Mediterranean diet that focused on a high intake of vegetables, legumes, fruits, fish, and healthy fats and a low intake of dairy products, meat, and saturated fatty acids.

Dementia diagnoses were determined by memory clinic physicians. A subpopulation of 738 participants had analyses of cerebrospinal fluid (CSF) levels of amyloid-beta 42 when they were referred to the Skåne University Hospital in Malmö memory clinic after developing clinical signs of cognitive impairment.

The primary outcome was progression to all-cause dementia. Secondary outcomes were progression to Alzheimer's dementia and vascular dementia. Over a median follow-up of 19.8 years, 1,943 people (6.9%) were diagnosed with all-cause dementia.

A comparison of worst-versus-best adherence to conventional dietary recommendations showed no difference in risk of all-cause dementia (HR 0.93, 95% CI 0.81-1.08), Alzheimer's dementia (HR 1.03, 0.85-1.23) or vascular dementia (HR 0.93, 95% 0.69-1.26).

Likewise, worst-versus-best adherence to a modified Mediterranean diet did not lower the risk of developing all-cause dementia (HR 0.93, 95% 0.75-1.15), Alzheimer's dementia (HR 0.90, 95% 0.68-1.19) or vascular dementia (HR 1.00, 95% 0.65-1.55).

In sensitivity analyses, results were similar when excluding people who developed dementia within 5 years or people with diabetes. Neither conventional diet recommendations nor a modified Mediterranean diet had a significant association with abnormal CSF amyloid-beta markers.

The results come with several caveats, Glans and colleagues noted. Dietary data were collected only at baseline and dietary habits may have changed during the follow-up period. In addition, participants with CSF samples were not randomized, but were recruited based on clinical indications.

"Randomized controlled trials are needed to provide additional evidence regarding the potential role of diet in relation to Alzheimer's disease pathology," they wrote.

  • Judy George covers neurology and neuroscience news for MedPage Today, writing about brain aging, Alzheimer’s, dementia, MS, rare diseases, epilepsy, autism, headache, stroke, Parkinson’s, ALS, concussion, CTE, sleep, pain, and more. Follow

Disclosures

The study was funded by the Swedish Research Council, the Knut and Alice Wallenberg Foundation, the Marianne and Marcus Wallenberg Foundation, the Strategic Research Area MultiPark at Lund University, the Swedish Alzheimer Foundation, the Swedish Brain Foundation, the Parkinson Foundation of Sweden, the Konung Gustaf V:s och Drottning Victorias Frimurarestiftelse, the Skåne University Hospital Foundation, Regionalt Forskningsstöd, and the Swedish federal government.

Glans dislcosed no relationships with industry. Co-authors disclosed relationships with F. Hoffmann-La Roche, Biogen, Geras Solutions, AVID Radiopharmaceuticals, Eli Lilly, Eisai, GE Healthcare, Pfizer, Genentech, Siemens, Alzpath, and Cerveau.

Peters and Nacmias disclosed no relationships with industry.