Griffith University research indicates that patients suffering from allergic rhinitis, otherwise known as hay fever, can specifically benefit from probiotic supplements.
In a study funded by Winclove Probiotics, Griffith’s research team at the Menzies Health Institute QLD found eight weeks of supplementation with a specific multi-species probiotic reduced symptoms of allergic rhinitis and medication use.
This study published in the Journal Genes, found most allergy patients (64%) responded with a clinical improvement in their QoL score, otherwise known as the quality of life scale.
Whilst noting that not all people with allergies respond similarly, Dr. Pete Smith of Queensland Allergy Services and a member of the study team said, “our study may allow us to personalize probiotic treatment for individuals with seasonal allergic rhinitis.”
Dr. Nic West of Griffith University adds that the evidence basefor the role of probiotics in allergy continues to increase.
“The results from our study will allow us to conduct targeted research to find strategies people can use during the pollen season,” said Dr. West.
Hay fever is a chronic disorder that has a serious impact on quality of life for up to 30% of the general population. Current treatment options are costly and do not tackle the underlying cause of the disorder.
With the aim of helping sufferers the research team examined the differences in the immune system between responders and non-responders and are currently undertaking a clinical trial of the probiotic supplement that involves further immune profiling of individuals with hay fever.
https://madisonarealymesupportgroup.com/2018/01/03/the-invisible-universe-of-the-human-microbiome-msm/Recitas, author of “The Plan,” calls MSM the wonder supplement for your gut. It can alleviate allergy symptoms, helps with detoxification, eliminates free radicals, and improves cell permeability. She states that with given time, MSM will start to actually repair damage caused by leaky gut – a common problem with Lyme/MSIDS patients. It can also help the body’s ability to absorb nutrients from food. Many Lyme patients struggle with paralysis of the gut where the muscles of the stomach and intestines stop being efficient. MSM helps this muscle tone as well.
Summary: Gentamicin and G418, two aminoglycoside antibiotics, were effective at correcting genetic mutations associated with a specific form of frontotemporal dementia. The findings are promising for the treatment of frontotemporal dementia.Source: University of Kentucky
Researchers at the University of Kentucky’s College of Medicine have found that a class of antibiotics called aminoglycosides could be a promising treatment for frontotemporal dementia.
Results of their proof of concept study, which was a collaborative effort between UK’s Department of Molecular and Cellular Biochemistry and the University of California San Francisco’s Department of Pathology, were recently published in the journal, Human Molecular Genetics.
Frontotemporal dementia is the most common type of early onset dementia. It typically begins between ages 40 and 65 and affects the frontal and temporal lobes of the brain, which leads to behavior changes, difficulty speaking and writing, and memory deterioration.
A subgroup of patients with frontotemporal dementia have a specific genetic mutation that prevents brain cells from making a protein called progranulin. Although progranulin is not widely understood, its absence is linked to the disease.
A group led by Haining Zhu, a professor in UK’s Department of Molecular and Cellular Biochemistry, discovered that after aminoglycoside antibiotics were added to neuronal cells with this mutation, the cells started making the full-length progranulin protein by skipping the mutation.
“These patients’ brain cells have a mutation that prevents progranulin from being made. The team found that by adding a small antibiotic molecule to the cells, they could ‘trick’ the cellular machinery into making it,” said Matthew Gentry, a co-author of the study and the Antonio S. Turco Endowed Professor in the Department of Molecular and Cellular Biochemistry.
The researchers found two specific aminoglycoside antibiotics – Gentamicin and G418 – were both effective in fixing the mutation and making the functional progranulin protein. After adding Gentamicin or G418 molecules to the affected cells, the progranulin protein level was recovered up to about 50 to 60%.
These results could be promising to drug development. Currently, there are no effective therapies for any type of dementia.
After this preclinical proof of concept study, the next step is to study the antibiotics’ effects on mice with the mutation that causes frontotemporal dementia, Zhu says. Another focus is to possibly develop new compounds from Gentamicin and G418 that could be safer and more effective. Although Gentamicin is an FDA-approved medication, its clinical usage is limited as it is associated with a number of adverse side effects.
“If we can get the right resources and physician to work with, we could potentially repurpose this drug. This is an early stage of the study, but it provides an important proof of concept that these aminoglycoside antibiotics or their derivatives can be a therapeutic avenue for frontotemporal dementia,” said Zhu.
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Frontotemporal dementia nonsense mutation of progranulin rescued by aminoglycosides
Frontotemporal dementia (FTD) is an early onset dementia and is characterized by progressive atrophy of the frontal and/or temporal lobes. FTD is highly heritable with mutations in progranulin accounting for 5-26% of cases in different populations. Progranulin is involved in endocytosis, secretion and lysosomal processes, but its function under physiological and pathological conditions remains to be defined. Many FTD-causing nonsense progranulin mutations contain a premature termination codon (PTC), thus progranulin haploinsufficiency has been proposed as a major disease mechanism. Currently, there is no effective FTD treatment or therapy.
What causes Alzheimer’s? Not toxic amyloid, new study suggests
Many researchers have argued that the accumulation of toxic beta-amyloid in the brain causes Alzheimer’s. However, a new study offers some evidence contradicting this sequence.
New research is questioning the predominant hypothesis that a buildup of beta-amyloid causes Alzheimer’s disease.
Yet, researchers are still at a loss as to why this condition — which is characterized by memory impairment and many other cognitive problems — occurs in the first place. And until they fully understand the cause, investigators will remain unable to devise a cure.
So far, the prevailing hypothesis among experts has been that the excessive accumulation of a potentially toxic protein — beta-amyloid — in the brain causes Alzheimer’s.
Researchers have argued that beta-amyloid plaques disrupt the communication between brain cells, potentially leading to cognitive function problems.
Now, a new study from the University of California San Diego School of Medicine and the Veterans Affairs San Diego Healthcare System suggests that while the buildup of beta-amyloid has associations with Alzheimer’s, it may not actually cause the condition.
In a study paper that appears in the journal Neurology, the researchers explain what led them to reach this conclusion.
“The scientific community has long thought that amyloid drives the neurodegeneration and cognitive impairment associated with Alzheimer’s disease,” says senior author Prof. Mark Bondi.
He notes that “[t]hese findings, in addition to other work in our lab, suggest that this is likely not the case for everyone and that sensitive neuropsychological measurement strategies capture subtle cognitive changes much earlier in the disease process than previously thought possible.”
What comes first?
In their study, the researchers worked with a total of 747 participants with different levels of cognitive health. All of the study participants agreed to undergo neuropsychological assessments, as well as PET and MRI brain scans.
Of the participants, 305 were cognitively healthy, 289 had mild cognitive impairment, and 153 displayed markers of what the investigators call “objectively-defined subtle cognitive difficulties (Obj-SCD).”
Experts define mild cognitive impairment as a state of cognitive impairment that is more severe than what one would normally experience with age, but not yet severe enough for a dementiadiagnosis.
But what are Obj-SCD? In their paper, the investigators define them as “difficulties or inefficiencies on some sensitive cognitive tasks even though the overall neuropsychological profile is in the normal range.”
That is, they are a measurement of experienced, subtle cognitive functioning problems that occur in the absence of any visible signs of brain or psychological issues. To find out whether someone is experiencing Obj-SCD, researchers assess, among other factors, how efficiently that person can learn and retain new information.
Previous research has suggested that individuals with Obj-SCD are at a higher risk of mild cognitive impairment and forms of dementia.
In the current study, Prof. Bondi and the team found that beta-amyloid built up at a faster rate in the participants with Obj-SCD compared with those who were deemed cognitively healthy. Moreover, brain scans of people with Obj-SCD showed that these individuals experienced a thinning of brain matter in a region called the entorhinal cortex.
Past research has shown that the entorhinal cortex decreases in volume in people with Alzheimer’s disease. This is significant because this brain region plays a role in memory and spatial orientation.
The researchers also found that while people with mild cognitive impairment had higher quantities of beta-amyloid in their brains at the beginning of the study, this protein did not seem to build up any faster in these participants than it did in cognitively healthy individuals.
But why do the current findings potentially contradict a decades-old hypothesis about the development of Alzheimer’s? Prof. Bondi explains:
“This work […] suggests that cognitive changes may be occurring before significant levels of amyloid have accumulated. It seems like we may need to focus on treatment targets of pathologies other than amyloid, such as tau, that are more highly associated with the thinking and memory difficulties that impact people’s lives.”
“While the emergence of biomarkers of Alzheimer’s disease has revolutionized research and our understanding of how the disease progresses, many of these biomarkers continue to be highly expensive, inaccessible for clinical use, or not available to those with certain medical conditions,” adds first author Kelsey Thomas, Ph.D.
The new study’s findings could help change that by refocusing the research approach on more subtle markers of Alzheimer’s, such as those assessing for Obj-SCD.
“A method of identifying individuals at risk for progression to [Alzheimer’s disease] using neuropsychological measures has the potential to improve early detection in those who may otherwise not be eligible for more expensive or invasive screening,” says Thomas.
Purpose: To provide a comprehensive review on rare and emerging micro-organisms causing infectious keratitis.
Material and Methods: A literature search was performed using PubMed Medline, Cochrane Library Database, EMBASE and Scopus (1960 onwards), using the terms: keratitis caused by rare pathogens; mycotic keratitis; fungal keratitis; bacterial keratitis; infectious keratitis; infective keratitis; atypical fungal keratitis; fungal keratitis caused by rare organisms; fungal keratitis caused by rare ocular pathogen; atypical bacterial keratitis; bacterial keratitis caused by rare organisms; bacterial keratitis caused by rare ocular pathogen. All relevant articles were included in this review.
Results: A total of 1232 articles matched our search strategy of which 124 articles were included in this mini-review. The rare and emerging bacteria causing keratitis include atypical mycobacteria, Nocardia spp., Chrysebacterium spp., Delftia acidovorans, Kocuria spp., Enterococcus spp., Bartonella henslae, Achromobacter spp. and others. The rare and emerging fungi causing keratitis include Pythium spp., Alternaria spp., Acremonium spp., Cladosporium spp., Curvularia spp., Bipolaris spp., Microsporidia spp., Pseudallescheria spp., Colletotrichum spp., and others. The clinical presentation of these cases is variable. While a few organisms produce characteristic clinical features, rest present similar to bacterial or fungal keratitis with variable response to routine treatment. A strong degree of suspicion is therefore essential for its diagnosis. Special investigations like polymerase chain reaction, gene sequencing, mass spectroscopy and enzyme-linked immunosorbent assay are required for accurate identification of these organisms. Culture-sensitivity is extremely useful as drug resistance to routinely used anti-microbial drugs is common. Prognosis is usually poor for keratitis with Pythium spp., Pseudallescheria spp., Arthrographis spp., Purpureocillium spp., Kociria spp. and Achromobacter spp.
Conclusion: Keratitis caused by rare and emerging micro-organisms must be suspected in cases where the infection runs an unusual course or shows poor response to standard anti-microbial drugs. Early diagnosis and timely treatment hold the key for good outcome.
BROAD RANGE OF PRESENTATIONS FOR LYME CARDITIS CASES
In their article “Risk factors for Lyme Carditis: A case-control study,” published in Preventive Cardiology, researchers from Stony Brook University Hospital described a wide range of Lyme carditis cases seen between 2010 – 2016.¹ Out of 247 patients admitted for Lyme disease, 18 met the inclusion criteria for Lyme carditis.
“[Lyme carditis] is caused by direct invasion of myocardial tissue by spirochetes and an immunological host response causing lymphocyte inflammation,” writes Marcos.¹
Furthermore, “B. burgdorferi has a predisposition to cause inflammation of the atrioventricular (AV) node resulting in variable conduction abnormalities.”
The 18 patients with possible Lyme carditis were predominantly Caucasian males with a mean age of 44.5 years (range was 24-79).
All of the patients met the CDC surveillance case definition for Lyme disease. One patient had an erythema migrans (EM) rash with negative blood tests.
The remaining 17 individuals had 2-3 IgM specific bands for Lyme disease. Of these, 5 presented with an EM rash and 11 had 5 or more IgG bands, explains Marcos.
“The most common symptoms at presentation were chest tightness, dizziness, and dyspnea on exertion and symptoms had been present for 4-30 days,” writes Marcos.
The 18 patients exhibited a wide range of abnormal EKG findings:
4 – AV block (2nd and 1st degree AV block)
6 – Right bundle branch conduction abnormalities
2 – New onset of atrial fibrillation
3 – T wave inversion
1 – Sinus bradycardia with ST elevation
2 – Prolonged QT interval
The authors were not able to address the outcome as the study was retrospective.
Marcos and colleagues were able to find a growing number of Lyme carditis cases in the literature. The most common presentation involved atrioventricular conduction abnormalities. Others included: right bundle branch block (RBBB), left bundle branch block (LBBB), widening of the QRS complex, AV dissociation, atrial fibrillation, ventricular dysfunction, fulminant myocarditis, and cardiac arrest.
“The spectrum of ECG abnormalities in [Lyme disease] may be broader than that previously suspected,” the authors conclude. “Clinicians should be aware of these ECG abnormalities that may be a sign of [Lyme carditis] in hyperendemic areas.”
“Fatal Lyme carditis caused by the spirochete Borrelia burgdorferi rarely is identified. Here, we describe the pathologic, immunohistochemical,and molecular findings of five case patients.”
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