Amyloid beta is an antibiotic protein component of the innate immune system.
Are Infections to Blame for Alzheimer’s Disease?
An interview with Robert D. Moir, PhD and Dale Bredesen, MD.
https://www.peoplespharmacy.com/article ... er-disease
Pharmaceutical scientists have been striving to get amyloid plaques out of the brain, but new research suggests that amyloid may be acting to protect the brain from microbes. What are the implications.
With nearly six million Americans living with Alzheimer’s disease, this condition is a serious public health problem. It robs people of their memories, their ability to function independently and even their very identities.
When Alois Alzheimer published the first report on the brain disease that was later named for him, he described distinctive plaques and neurofibrillary tangles in the brain. That was in 1906. Ever since then, scientists have been trying to figure out what causes those plaques and tangles and how we can prevent them.
Researchers have known for decades that the plaques that characterize Alzheimer’s disease contain a lot of beta-amyloid peptide. They call it A-beta. Drug companies have been struggling to find pharmaceuticals that can clear this bad actor out of the brain. Unfortunately, the agents they have tested so far have been disappointing at best.
What Is A-Beta Doing in the Brain?
Neuroscientists have assumed that A-beta is toxic to neurons, and that it has no legitimate business in the brain. But that assumption may be mistaken.
New research demonstrates that A-beta is part of the brain’s immune defenses. It seems that it has played an important role in protecting the brain from infection throughout human evolution.
The Microbiome of the Brain:
Our guest, Robert Moir, and his colleagues found that the brain has a complex, previously unsuspected, microbiome. The A-beta compound that makes up amyloid plaques is a powerful antibiotic–100 times more potent than penicillin.
He studied ways to find anti-inflammatory compounds that target innate immunity of the sort found in the brain. He suggested that all of us can help our brains by eating a heart-healthy diet (it’s good for the brain, too), staying fit with regular exercise and drinking alcohol in moderation if at all.
If A-beta is actually acting to protect the brain, it could be a mistake to try to get rid of it. Instead, perhaps we should figure out how to help it. Our second guest, Dr. Dale Bredesen, also has a number of suggestions on how we can do that and reduce our risk of Alzheimer disease. He suggests measuring ketones and aiming for a sweet spot between 1.5 and 4 millimoles of beta-hydroxy-butyrate.
NPR did an in-depth report on the possibility that Alzheimer disease is caused in part by infection and the immune system’s response on Sept. 9, 2018.
You may also be interested in this in-depth report of Dr. Moir’s research process in STAT.
This Week’s Guests:
We are sorry to note that Robert D. Moir, PhD, died of glioblastoma late in 2019. He was Assistant Professor in Neurology at Harvard Medical School and Assistant Professor in Neurology at MGH Neurology Research. His research focused on the biochemical and cellular mechanisms involved in neurodegeneration in Alzheimer’s disease and aging. You can find his publication on herpes virus and beta-amyloid in Neuron, July 11, 2018.
Dale Bredesen, MD, is an expert in the mechanisms of neurodegeneration and has served on the faculty at the University of California, San Francisco, and UCLA. He directed the program on Aging at the Burnham Institute prior to joining the Buck Institute for Research on Aging as its founding president and CEO. We spoke with him via Skype.
The brain’s microbiome
Re: The brain’s microbiome
Microbiome of the Eye
By Reena Mukamal
Reviewed By Russell N Van Gelder MD PhD, Natasha L Herz MD
Jan. 29, 2019
Your eyes have a microbiome, too
Microbiomes are communities of organisms including bacteria, fungi and viruses that live on and inside our bodies. Some are harmful and can cause infections, but many parts of the body’s microbiome are essential to good health. Sometimes, the microbiome activates the immune system to get rid of dangerous bacteria and prevent disease.
In addition to the well-known gut microbiome, your mouth, skin and eyes each have a unique microbiome. The ocular microbiome is a relatively new and emerging area of research and it may lead to new approaches for treatment and prevention of certain eye diseases and conditions.
The ocular microbiome is a relatively small population
The community of micro-organisms (flora) in the eye are found on the conjunctiva (the clear tissue covering the white part of your eye) and the cornea. Flora found in the eyelid and eyelashes are considered part of the skin microbiome. Compared to other bodily microbiomes, the ocular surface microbiome is sparsely occupied. If the skin is the Los Angeles of microbiomes, the eye is more like Wichita, Kansas, with roughly 1/100th the number of resident micro-organisms.
At first scientists believed there were many more bacteria living in the eye, but today they have confirmed that the core ocular surface microbiome for most people has just four species: Staphylococcus, Streptococcus, Propionibacterium and Corynebacterium. This bacterial population is probably so small because your tears are somewhat antimicrobial. Enzymes in tears break down bacterial cell walls and keep them from reproducing.
Microbiome imbalances may increase risk of eye diseases
In other microbiomes in the body, imbalances of the native species of bacteria have been shown to affect health and kickstart disease. In the gut, certain forms of colitis are caused by clostridium difficile (C. diff), which can grow unchecked when there is an imbalance of native, healthy bacteria. Researchers hypothesize that the ocular biome could similarly influence risk for conditions such as dry eye disease and endophthalmitis (a severe eye inflammation often caused by infection after eye surgery).
The ocular microbiome is also home to native viruses
In addition to bacteria, the healthy ocular surface frequently hosts some viruses, such as the torque teno virus (TTV). The TTV virus has been found in many cases of endophthalmitis but how it gets inside the eye to cause this condition is not yet clear. Other viruses that are part of healthy ocular microbiomes include the Merkel Cell Polyomavirus (MCP) and human papillomavirus (HPV). These viruses, which are usually undesirable, may serve as watchdogs in the ocular microbiome, alerting the immune system when other viruses pop up.
What microbiome research is being done and how will it influence eye health?
In the future, researchers plan to investigate the potential connection between the ocular microbiome and eye conditions that damage the ocular surface. These include chronic dry eye and blepharitis (bacteria and oily flakes at the base of the eyelashes).
Other areas of upcoming investigation include:
analysis of the molecular biology of endophthalmitis
eye surface inflammation, such as viral conjunctivitis; and
the ocular microbiome’s possible impact on contact lens-related inflammation or infection.
Today, we are just at the beginning of understanding what makes up a healthy ocular microbiome. There is much more to discover.
By Reena Mukamal
Reviewed By Russell N Van Gelder MD PhD, Natasha L Herz MD
Jan. 29, 2019
Your eyes have a microbiome, too
Microbiomes are communities of organisms including bacteria, fungi and viruses that live on and inside our bodies. Some are harmful and can cause infections, but many parts of the body’s microbiome are essential to good health. Sometimes, the microbiome activates the immune system to get rid of dangerous bacteria and prevent disease.
In addition to the well-known gut microbiome, your mouth, skin and eyes each have a unique microbiome. The ocular microbiome is a relatively new and emerging area of research and it may lead to new approaches for treatment and prevention of certain eye diseases and conditions.
The ocular microbiome is a relatively small population
The community of micro-organisms (flora) in the eye are found on the conjunctiva (the clear tissue covering the white part of your eye) and the cornea. Flora found in the eyelid and eyelashes are considered part of the skin microbiome. Compared to other bodily microbiomes, the ocular surface microbiome is sparsely occupied. If the skin is the Los Angeles of microbiomes, the eye is more like Wichita, Kansas, with roughly 1/100th the number of resident micro-organisms.
At first scientists believed there were many more bacteria living in the eye, but today they have confirmed that the core ocular surface microbiome for most people has just four species: Staphylococcus, Streptococcus, Propionibacterium and Corynebacterium. This bacterial population is probably so small because your tears are somewhat antimicrobial. Enzymes in tears break down bacterial cell walls and keep them from reproducing.
Microbiome imbalances may increase risk of eye diseases
In other microbiomes in the body, imbalances of the native species of bacteria have been shown to affect health and kickstart disease. In the gut, certain forms of colitis are caused by clostridium difficile (C. diff), which can grow unchecked when there is an imbalance of native, healthy bacteria. Researchers hypothesize that the ocular biome could similarly influence risk for conditions such as dry eye disease and endophthalmitis (a severe eye inflammation often caused by infection after eye surgery).
The ocular microbiome is also home to native viruses
In addition to bacteria, the healthy ocular surface frequently hosts some viruses, such as the torque teno virus (TTV). The TTV virus has been found in many cases of endophthalmitis but how it gets inside the eye to cause this condition is not yet clear. Other viruses that are part of healthy ocular microbiomes include the Merkel Cell Polyomavirus (MCP) and human papillomavirus (HPV). These viruses, which are usually undesirable, may serve as watchdogs in the ocular microbiome, alerting the immune system when other viruses pop up.
What microbiome research is being done and how will it influence eye health?
In the future, researchers plan to investigate the potential connection between the ocular microbiome and eye conditions that damage the ocular surface. These include chronic dry eye and blepharitis (bacteria and oily flakes at the base of the eyelashes).
Other areas of upcoming investigation include:
analysis of the molecular biology of endophthalmitis
eye surface inflammation, such as viral conjunctivitis; and
the ocular microbiome’s possible impact on contact lens-related inflammation or infection.
Today, we are just at the beginning of understanding what makes up a healthy ocular microbiome. There is much more to discover.
https://www.eboro.cz
Re: The brain’s microbiome
Do gut bacteria make a second home in our brains?
Preliminary finding turns heads at neuroscience meeting.
https://www.science.org/content/article ... our-brains
Images of human brain slices reveal bacteria, shown here to the left of a blood vessel—tantalizing but preliminary evidence of a "brain microbiome."
SAN DIEGO, CALIFORNIA—We know the menagerie of microbes in the gut has powerful effects on our health. Could some of these same bacteria be making a home in our brains? A poster presented here this week at the annual meeting of the Society for Neuroscience drew attention with high-resolution microscope images of bacteria apparently penetrating and inhabiting the cells of healthy human brains. The work is preliminary, and its authors are careful to note that their tissue samples, collected from cadavers, could have been contaminated. But to many passersby in the exhibit hall, the possibility that bacteria could directly influence processes in the brain—including, perhaps, the course of neurological disease—was exhilarating.
"This is the hit of the week," said neuroscientist Ronald McGregor of the University of California, Los Angeles, who was not involved in the work. "It's like a whole new molecular factory [in the brain] with its own needs. … This is mind-blowing."
The brain is a protected environment, partially walled off from the contents of the bloodstream by a network of cells that surround its blood vessels. Bacteria and viruses that manage to penetrate this blood-brain barrier can cause life-threatening inflammation. Some research has suggested distant microbes—those living in our gut—might affect mood and behavior and even the risk of neurological disease, but by indirect means. For example, a disruption in the balance of gut microbiomes could increase the production of a rogue protein that may cause Parkinson's disease if it travels up the nerve connecting the gut to the brain.
- - - - - - - - - - - - - - - - -
RNA sequencing revealed that most of the bacteria were from three phyla common to the gut: Firmicutes, Proteobacteria, and Bacteroidetes. Roberts doesn't know how these bacteria could have gotten into the brain. They may have crossed from blood vessels, traveling up nerves from the gut, or even come in through the nose. And she can't say much about whether they're helpful or harmful. She saw no signs of inflammation to suggest they were causing harm, but hasn't yet quantified them or systematically compared the schizophrenic and healthy brains. If it turns out that there are major differences, future research could examine how this proposed "brain microbiome" could maintain or threaten the health of the brain.
In the initial survey of the electron micrographs, Roberts's team observed that resident bacteria had puzzling preferences. They seemed to inhabit star-shaped cells called astrocytes, which interact with and support neurons. In particular, the microbes clustered in and around the ends of astrocytes that encircle blood vessels at the blood-brain barrier. They also appeared to be more abundant around the long projections of neurons that are sheathed in the fatty substance called myelin. Roberts can't explain those preferences but wonders whether the bacteria are attracted to fat and sugar in these brain cells.
[continued]
Preliminary finding turns heads at neuroscience meeting.
https://www.science.org/content/article ... our-brains
Images of human brain slices reveal bacteria, shown here to the left of a blood vessel—tantalizing but preliminary evidence of a "brain microbiome."
SAN DIEGO, CALIFORNIA—We know the menagerie of microbes in the gut has powerful effects on our health. Could some of these same bacteria be making a home in our brains? A poster presented here this week at the annual meeting of the Society for Neuroscience drew attention with high-resolution microscope images of bacteria apparently penetrating and inhabiting the cells of healthy human brains. The work is preliminary, and its authors are careful to note that their tissue samples, collected from cadavers, could have been contaminated. But to many passersby in the exhibit hall, the possibility that bacteria could directly influence processes in the brain—including, perhaps, the course of neurological disease—was exhilarating.
"This is the hit of the week," said neuroscientist Ronald McGregor of the University of California, Los Angeles, who was not involved in the work. "It's like a whole new molecular factory [in the brain] with its own needs. … This is mind-blowing."
The brain is a protected environment, partially walled off from the contents of the bloodstream by a network of cells that surround its blood vessels. Bacteria and viruses that manage to penetrate this blood-brain barrier can cause life-threatening inflammation. Some research has suggested distant microbes—those living in our gut—might affect mood and behavior and even the risk of neurological disease, but by indirect means. For example, a disruption in the balance of gut microbiomes could increase the production of a rogue protein that may cause Parkinson's disease if it travels up the nerve connecting the gut to the brain.
- - - - - - - - - - - - - - - - -
RNA sequencing revealed that most of the bacteria were from three phyla common to the gut: Firmicutes, Proteobacteria, and Bacteroidetes. Roberts doesn't know how these bacteria could have gotten into the brain. They may have crossed from blood vessels, traveling up nerves from the gut, or even come in through the nose. And she can't say much about whether they're helpful or harmful. She saw no signs of inflammation to suggest they were causing harm, but hasn't yet quantified them or systematically compared the schizophrenic and healthy brains. If it turns out that there are major differences, future research could examine how this proposed "brain microbiome" could maintain or threaten the health of the brain.
In the initial survey of the electron micrographs, Roberts's team observed that resident bacteria had puzzling preferences. They seemed to inhabit star-shaped cells called astrocytes, which interact with and support neurons. In particular, the microbes clustered in and around the ends of astrocytes that encircle blood vessels at the blood-brain barrier. They also appeared to be more abundant around the long projections of neurons that are sheathed in the fatty substance called myelin. Roberts can't explain those preferences but wonders whether the bacteria are attracted to fat and sugar in these brain cells.
[continued]
Re: The brain’s microbiome
From the 2018 Society for Neuroscience Meeting:
The human brain microbiome; there are bacteria in our brains!
Neuroscience San Diego CA, Rosalinda Roberts, 2018
Abstract:
The gut-brain microbiome has received an abundance of attention recently. It is thought that gut microbiota can influence brain function and behavior, but how that happens is still unknown. It has been proposed that bacteria can enter the brain through the blood brain barrier, and/or via nerves that innervate the gut. Here we show the presence of bacteria in the human and mouse brain under noninfectious or nontraumatic conditions. We first found the bacteria, identified by morphological criteria, in ultrastructural samples of human postmortem brain (n=34 cases). We did serial section analysis for identification and quantification. All cases contained bacteria in varying amounts. Bacteria were rod shaped, and contained a capsule, nucleoid, ribosomes and vacuoles. The average diameter of the short axis was 0.496um. Many were segmented, with the long axis averaging approximately 1.78um between segments. Others did not appear to be segmented and were approximately 0.866um in the long axis. The vast majority of the profiles had a thick capsule of approximately 100nm. The density of the bacteria varied according to the brain region, with abundant bacteria in the substantia nigra, hippocampus and prefrontal cortex but sparse numbers in the striatum. Bacteria were present in intracellular locations, predominantly in astrocytic end feet at the blood brain barrier, dendrites and the soma of glial cells. They were also abundant adjacent to and within myelinated axons. To address the possibility that the bacteria in human tissue was a result of postmortem artifact, we examined mouse brains that were fixed immediately at death (n=10); there were abundant bacteria in similar intracellular locations. To eliminate the possibility that the presence of bacteria was due to contamination, we examined germ free mouse brains (n=4) processed in an identical way; we did not detect any bacteria. The observation that the location of the bacteria was highly specific and deep within the specimens also argues against contamination. Interestingly, there were no structural signs of inflammation in any of the brains examined. It is presently unclear the route of entry bacteria take to the brain, but the evidence of them in axons and at the blood brain barrier supports previous speculation.
The human brain microbiome; there are bacteria in our brains!
Neuroscience San Diego CA, Rosalinda Roberts, 2018
Abstract:
The gut-brain microbiome has received an abundance of attention recently. It is thought that gut microbiota can influence brain function and behavior, but how that happens is still unknown. It has been proposed that bacteria can enter the brain through the blood brain barrier, and/or via nerves that innervate the gut. Here we show the presence of bacteria in the human and mouse brain under noninfectious or nontraumatic conditions. We first found the bacteria, identified by morphological criteria, in ultrastructural samples of human postmortem brain (n=34 cases). We did serial section analysis for identification and quantification. All cases contained bacteria in varying amounts. Bacteria were rod shaped, and contained a capsule, nucleoid, ribosomes and vacuoles. The average diameter of the short axis was 0.496um. Many were segmented, with the long axis averaging approximately 1.78um between segments. Others did not appear to be segmented and were approximately 0.866um in the long axis. The vast majority of the profiles had a thick capsule of approximately 100nm. The density of the bacteria varied according to the brain region, with abundant bacteria in the substantia nigra, hippocampus and prefrontal cortex but sparse numbers in the striatum. Bacteria were present in intracellular locations, predominantly in astrocytic end feet at the blood brain barrier, dendrites and the soma of glial cells. They were also abundant adjacent to and within myelinated axons. To address the possibility that the bacteria in human tissue was a result of postmortem artifact, we examined mouse brains that were fixed immediately at death (n=10); there were abundant bacteria in similar intracellular locations. To eliminate the possibility that the presence of bacteria was due to contamination, we examined germ free mouse brains (n=4) processed in an identical way; we did not detect any bacteria. The observation that the location of the bacteria was highly specific and deep within the specimens also argues against contamination. Interestingly, there were no structural signs of inflammation in any of the brains examined. It is presently unclear the route of entry bacteria take to the brain, but the evidence of them in axons and at the blood brain barrier supports previous speculation.
Re: The brain’s microbiome
Microbiota from Alzheimer's patients induce deficits in cognition and hippocampal neurogenesis
Brain. 2023 Oct 18:awad303.
Alzheimer's disease is a complex neurodegenerative disorder leading to a decline in cognitive function and mental health. Recent research has positioned the gut microbiota as an important susceptibility factor in Alzheimer's disease by showing specific alterations in the gut microbiome composition of Alzheimer's patients and in rodent models. However, it is unknown whether gut microbiota alterations are causal in the manifestation of Alzheimer's symptoms. To understand the involvement of Alzheimer's patient gut microbiota in host physiology and behaviour, we transplanted faecal microbiota from Alzheimer's patients and age-matched healthy controls into microbiota-depleted young adult rats. We found impairments in behaviours reliant on adult hippocampal neurogenesis, an essential process for certain memory functions and mood, resulting from Alzheimer's patient transplants. Notably, the severity of impairments correlated with clinical cognitive scores in donor patients. Discrete changes in the rat caecal and hippocampal metabolome were also evident. As hippocampal neurogenesis cannot be measured in living humans but is modulated by the circulatory systemic environment, we assessed the impact of the Alzheimer's systemic environment on proxy neurogenesis readouts. Serum from Alzheimer's patients decreased neurogenesis in human cells in vitro and were associated with cognitive scores and key microbial genera. Our findings reveal for the first time, that Alzheimer's symptoms can be transferred to a healthy young organism via the gut microbiota, confirming a causal role of gut microbiota in Alzheimer's disease, and highlight hippocampal neurogenesis as a converging central cellular process regulating systemic circulatory and gut-mediated factors in Alzheimer's.
Brain. 2023 Oct 18:awad303.
Alzheimer's disease is a complex neurodegenerative disorder leading to a decline in cognitive function and mental health. Recent research has positioned the gut microbiota as an important susceptibility factor in Alzheimer's disease by showing specific alterations in the gut microbiome composition of Alzheimer's patients and in rodent models. However, it is unknown whether gut microbiota alterations are causal in the manifestation of Alzheimer's symptoms. To understand the involvement of Alzheimer's patient gut microbiota in host physiology and behaviour, we transplanted faecal microbiota from Alzheimer's patients and age-matched healthy controls into microbiota-depleted young adult rats. We found impairments in behaviours reliant on adult hippocampal neurogenesis, an essential process for certain memory functions and mood, resulting from Alzheimer's patient transplants. Notably, the severity of impairments correlated with clinical cognitive scores in donor patients. Discrete changes in the rat caecal and hippocampal metabolome were also evident. As hippocampal neurogenesis cannot be measured in living humans but is modulated by the circulatory systemic environment, we assessed the impact of the Alzheimer's systemic environment on proxy neurogenesis readouts. Serum from Alzheimer's patients decreased neurogenesis in human cells in vitro and were associated with cognitive scores and key microbial genera. Our findings reveal for the first time, that Alzheimer's symptoms can be transferred to a healthy young organism via the gut microbiota, confirming a causal role of gut microbiota in Alzheimer's disease, and highlight hippocampal neurogenesis as a converging central cellular process regulating systemic circulatory and gut-mediated factors in Alzheimer's.
Re: The brain’s microbiome
2023 Oct 19
College of Medicine, Alfaisal University, Riyadh, Saudi Arabia
Brain-inhabiting bacteria and neurodegenerative diseases: the "brain microbiome" theory
https://pubmed.ncbi.nlm.nih.gov/37927338/
Abstract
Controversies surrounding the validity of the toxic proteinopathy theory of Alzheimer's disease have led the scientific community to seek alternative theories in the pathogenesis of neurodegenerative disorders (ND). Recent studies have provided evidence of a microbiome in the central nervous system. Some have hypothesized that brain-inhabiting organisms induce chronic neuroinflammation, leading to the development of a spectrum of NDs. Bacteria such as Chlamydia pneumoniae, Helicobacter pylori, and Cutibacterium acnes have been found to inhabit the brains of ND patients. Furthermore, several fungi, including Candida and Malassezia species, have been identified in the central nervous system of these patients. However, there remains several limitations to the brain microbiome hypothesis. Varying results across the literature, concerns regarding sample contamination, and the presence of exogenous deoxyribonucleic acids have led to doubts about the hypothesis. These results provide valuable insight into the pathogenesis of NDs. Herein, we provide a review of the evidence for and against the brain microbiome theory and describe the difficulties facing the hypothesis. Additionally, we define possible mechanisms of bacterial invasion of the brain and organism-related neurodegeneration in NDs and the potential therapeutic premises of this theory.
College of Medicine, Alfaisal University, Riyadh, Saudi Arabia
Brain-inhabiting bacteria and neurodegenerative diseases: the "brain microbiome" theory
https://pubmed.ncbi.nlm.nih.gov/37927338/
Abstract
Controversies surrounding the validity of the toxic proteinopathy theory of Alzheimer's disease have led the scientific community to seek alternative theories in the pathogenesis of neurodegenerative disorders (ND). Recent studies have provided evidence of a microbiome in the central nervous system. Some have hypothesized that brain-inhabiting organisms induce chronic neuroinflammation, leading to the development of a spectrum of NDs. Bacteria such as Chlamydia pneumoniae, Helicobacter pylori, and Cutibacterium acnes have been found to inhabit the brains of ND patients. Furthermore, several fungi, including Candida and Malassezia species, have been identified in the central nervous system of these patients. However, there remains several limitations to the brain microbiome hypothesis. Varying results across the literature, concerns regarding sample contamination, and the presence of exogenous deoxyribonucleic acids have led to doubts about the hypothesis. These results provide valuable insight into the pathogenesis of NDs. Herein, we provide a review of the evidence for and against the brain microbiome theory and describe the difficulties facing the hypothesis. Additionally, we define possible mechanisms of bacterial invasion of the brain and organism-related neurodegeneration in NDs and the potential therapeutic premises of this theory.
https://www.eboro.cz
Re: The brain’s microbiome
Here's a small double blind trial where Alzheimer's patients were given a probiotic. The treatment group had significant improvements in several disease markers. Here are some examples, improvement in Mini Mental State Examination (MMSE) scores, C reactive protein (a marker of inflammation) decreased, serum triglycerides decreased, malondialdehyde (MDA, a marker of inflammation) decreased and others as well.
Effect of Probiotic Supplementation on Cognitive Function and Metabolic Status in Alzheimer's Disease: A Randomized, Double-Blind and Controlled Trial
Front Aging Neurosci. 2016 Nov 10:8:256.
Alzheimer's disease (AD) is associated with severe cognitive impairments as well as some metabolic defects. Scant studies in animal models indicate a link between probiotics and cognitive function. This randomized, double-blind, and controlled clinical trial was conducted among 60 AD patients to assess the effects of probiotic supplementation on cognitive function and metabolic status. The patients were randomly divided into two groups (n = 30 in each group) treating with either milk (control group) or a mixture of probiotics (probiotic group). The probiotic supplemented group took 200 ml/day probiotic milk containing Lactobacillus acidophilus, Lactobacillus casei, Bifidobacterium bifidum, and Lactobacillus fermentum (2 × 109 CFU/g for each) for 12 weeks. Mini-mental state examination (MMSE) score was recorded in all subjects before and after the treatment. Pre- and post-treatment fasting blood samples were obtained to determine the related markers. After 12 weeks intervention, compared with the control group (-5.03% ± 3.00), the probiotic treated (+27.90% ± 8.07) patients showed a significant improvement in the MMSE score (P <0.001). In addition, changes in plasma malondialdehyde (-22.01% ± 4.84 vs. +2.67% ± 3.86 μmol/L, P <0.001), serum high-sensitivity C-reactive protein (-17.61% ± 3.70 vs. +45.26% ± 3.50 μg/mL, P <0.001), homeostasis model of assessment-estimated insulin resistance (+28.84% ± 13.34 vs. +76.95% ± 24.60, P = 0.002), Beta cell function (+3.45% ± 10.91 vs. +75.62% ± 23.18, P = 0.001), serum triglycerides (-20.29% ± 4.49 vs. -0.16% ± 5.24 mg/dL, P = 0.003), and quantitative insulin sensitivity check index (-1.83 ± 1.26 vs. -4.66 ± 1.70, P = 0.006) in the probiotic group were significantly varied compared to the control group. We found that the probiotic treatment had no considerable effect on other biomarkers of oxidative stress and inflammation, fasting plasma glucose, and other lipid profiles. Overall, the current study demonstrated that probiotic consumption for 12 weeks positively affects cognitive function and some metabolic statuses in the AD patients.
Free full text.
Effect of Probiotic Supplementation on Cognitive Function and Metabolic Status in Alzheimer's Disease: A Randomized, Double-Blind and Controlled Trial
Front Aging Neurosci. 2016 Nov 10:8:256.
Alzheimer's disease (AD) is associated with severe cognitive impairments as well as some metabolic defects. Scant studies in animal models indicate a link between probiotics and cognitive function. This randomized, double-blind, and controlled clinical trial was conducted among 60 AD patients to assess the effects of probiotic supplementation on cognitive function and metabolic status. The patients were randomly divided into two groups (n = 30 in each group) treating with either milk (control group) or a mixture of probiotics (probiotic group). The probiotic supplemented group took 200 ml/day probiotic milk containing Lactobacillus acidophilus, Lactobacillus casei, Bifidobacterium bifidum, and Lactobacillus fermentum (2 × 109 CFU/g for each) for 12 weeks. Mini-mental state examination (MMSE) score was recorded in all subjects before and after the treatment. Pre- and post-treatment fasting blood samples were obtained to determine the related markers. After 12 weeks intervention, compared with the control group (-5.03% ± 3.00), the probiotic treated (+27.90% ± 8.07) patients showed a significant improvement in the MMSE score (P <0.001). In addition, changes in plasma malondialdehyde (-22.01% ± 4.84 vs. +2.67% ± 3.86 μmol/L, P <0.001), serum high-sensitivity C-reactive protein (-17.61% ± 3.70 vs. +45.26% ± 3.50 μg/mL, P <0.001), homeostasis model of assessment-estimated insulin resistance (+28.84% ± 13.34 vs. +76.95% ± 24.60, P = 0.002), Beta cell function (+3.45% ± 10.91 vs. +75.62% ± 23.18, P = 0.001), serum triglycerides (-20.29% ± 4.49 vs. -0.16% ± 5.24 mg/dL, P = 0.003), and quantitative insulin sensitivity check index (-1.83 ± 1.26 vs. -4.66 ± 1.70, P = 0.006) in the probiotic group were significantly varied compared to the control group. We found that the probiotic treatment had no considerable effect on other biomarkers of oxidative stress and inflammation, fasting plasma glucose, and other lipid profiles. Overall, the current study demonstrated that probiotic consumption for 12 weeks positively affects cognitive function and some metabolic statuses in the AD patients.
Free full text.
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