inflammation in the brain Archives - Amazing Health Advances

Glyphosate Exposure Linked to Lasting Brain Inflammation

The AHA! Team — Mon, 20 Jan 2025 06:04:19 +0000

Arizona State University via News-Medical – The human brain is an incredibly adaptable organ, often able to heal itself even from significant trauma. The human brain is an incredibly adaptable organ, often able to heal itself even from significant trauma. Yet for the first time, new research shows even brief contact with a common herbicide can cause lasting damage to the brain, which may persist long after direct exposure ends. In a groundbreaking new study, Arizona State University researcher Ramon Velazquez and his colleagues at the Translational Genomics Research Institute (TGen), part of City of Hope, demonstrate that mice exposed to the herbicide glyphosate develop significant brain inflammation, which is associated with neurodegenerative disease. The findings suggest the brain may be much more susceptible to the damaging effects of the herbicide than previously thought. Glyphosate is one of the most pervasive herbicides used in the U.S. and worldwide. The research, which appears today in the Journal of Neuroinflammation, identifies an association between glyphosate exposure in mice and symptoms of neuroinflammation, as well as accelerated Alzheimer’s disease-like pathology. This study tracks both the presence and impact of glyphosate’s byproducts in the brain long after exposure ends, showing an array of persistent, damaging effects on brain health. The research, appeared in the Journal of Neuroinflammation Glyphosate exposure in mice also resulted in premature death and anxiety-like behaviors, which replicates findings by others examining glyphosate exposure in rodents. Further, the scientists discovered these symptoms persisted even after a 6-month recovery period during which exposure was discontinued. Additionally, the investigation demonstrated that a byproduct of glyphosate – aminomethylphosphonic acid – accumulated in brain tissue, raising serious concerns about the chemical’s safety for human populations. “Our work contributes to the growing literature highlighting the brain’s vulnerability to glyphosate. Given the increasing incidence of cognitive decline in the aging population, particularly in rural communities where exposure to glyphosate is more common due to large-scale farming, there is an urgent need for more basic research on the effects of this herbicide.” Ramon Velazquez, researcher, Arizona State University Velazquez is a researcher with the ASU-Banner Neurodegenerative Disease Research Center at the ASU Biodesign Institute and an assistant professor with the School of Life Sciences. He is joined by first author Samantha K. Bartholomew, a PhD candidate in the Velazquez Lab, other ASU colleagues, and co-senior author Patrick Pirrotte, associate professor with the Translational Genomics Research Institute (TGen) and researcher with the City of Hope Comprehensive Cancer Center in California. According to the Centers for Disease Research, farm laborers, landscape workers, and others employed in agriculture are more likely to be exposed to glyphosate through inhalation or skin contact. Additionally, the new findings suggest that ingestion of glyphosate residues on foods sprayed with the herbicide potentially poses a health hazard. Most people living in the U.S. have been exposed to glyphosate during their lifetime. “My hope is that our work drives further investigation into the effects of glyphosate exposure, which may lead to a reexamination of its long-term safety and perhaps spark discussion about other prevalent toxins in our environment that may affect the brain,” Bartholomew says. The team’s findings build on earlier ASU research that demonstrates a link between glyphosate exposure and a heightened risk for neurodegenerative disorders. The previous study showed that glyphosate crosses the blood-brain barrier, a protective layer that typically prevents potentially harmful substances from entering the brain. Once glyphosate crosses this barrier, it can interact with brain tissue and appears to contribute to neuroinflammation and other harmful effects on neural function. The EPA considers certain levels of glyphosate safe for human exposure, asserting that the chemical is minimally absorbed into the body and is primarily excreted unchanged. However, recent studies, including this one, indicate that glyphosate, and its major metabolite aminomethylphosphonic acid, can persist in the body and accumulate in brain tissue over time, raising questions about existing safety thresholds and whether glyphosate use is safe at all. Herbicide may attack more than weeds Glyphosate is the world’s most heavily applied herbicide, used on crops including corn, soybeans, sugar beets, alfalfa, cotton and wheat. Since the introduction of glyphosate-tolerant crops (genetically engineered to be sprayed with glyphosate without dying) in 1996, glyphosate usage has surged, with applications predominately in agricultural settings. The U.S. Geological Survey notes approximately 300 million pounds of glyphosate are used annually in the United States alone. Although glyphosate levels are regulated on foods imported into the United States, enforcement and specific limits can vary. Due to its widespread use, the chemical is found throughout the food chain. It persists in the air, accumulates in soils, and is found in surface and groundwater. Despite being considered safe by the EPA, the International Agency for Research on Cancer classifies glyphosate as “possibly carcinogenic to humans,” and emerging research, including this study, points to its potential role in worsening neurodegenerative diseases by contributing to pathologies, like those seen in Alzheimer’s disease. The chemical works by inhibiting a specific enzyme pathway in plants that is crucial for producing essential amino acids. However, its impact extends beyond the intended weed, grass and plant targets, negatively affecting the biological systems in mammals, as demonstrated by its persistence in brain tissue and its role in inflammatory processes. “Herbicides are used heavily and ubiquitously around the world,” says Pirrotte, associate professor in TGen’s Early Detection and Prevention Division, director of the Integrated Mass Spectrometry Shared Resource at TGen and City of Hope, and senior author of the paper. “These findings highlight that many chemicals we regularly encounter, previously considered safe, may pose potential health risks. However, further research is needed to fully assess the public health impact and identify safer alternatives.” Is glyphosate safe to use at all? The researchers hypothesized that glyphosate exposure would induce neuroinflammation in control mice and worsen neuroinflammation in Alzheimer’s model mice, causing elevated Amyloid-β and tau pathology and worsening spatial cognition after recovery. Amyloid-β and Tau are key proteins that comprise plaques and tau tangles, the classic diagnostic markers of Alzheimer’s disease. Plaques and tangles disrupt neural functioning and are directly linked to memory loss and cognitive decline. The experiments were conducted over 13 weeks, followed by a six-month recovery period. The main metabolite, aminomethylphosphonic acid, was detected in the brains of both normal and transgenic mice with Alzheimer’s pathology. Transgenic mice are genetically modified to carry genes that cause them to develop Alzheimer’s-like symptoms as they age. This allows researchers to study the progression and effects of the disease in a controlled laboratory setting. The researchers tested two levels of glyphosate exposure: a high dose, similar to levels used in earlier research, and a lower dose that is close to the limit used to establish the current acceptable dose in humans. This lower dose still led to harmful effects in the brains of mice, even after exposure ceased for months. While reports show that most Americans are exposed to glyphosate daily, these results show that even a short period could potentially cause neurological damage. Glyphosate caused a persistent increase in inflammatory markers in the brain and blood, even after the recovery period. This prolonged inflammation could drive the progression of neurodegenerative diseases, including Alzheimer’s, indicating even temporary glyphosate exposure can lead to enduring inflammatory processes that affect brain health. The data emphasizes that glyphosate exposure may be a significant health concern for human populations. The researchers stress the need for continued vigilance and intensified surveillance of glyphosate neurological and other long-term negative health effects. “Our goal is to identify environmental factors that contribute to the rising prevalence of cognitive decline and neurodegenerative diseases in our society,” Velazquez says. “By unveiling such factors, we can develop strategies to minimize exposures, ultimately improving the quality of life for the growing aging population.” The National Institutes on Aging, National Cancer Institute of the National Institutes of Health, and ASU Biodesign Institute funded this study. Source: Arizona State University Journal reference: Bartholomew, S. K., et al. (2024) Glyphosate exposure exacerbates neuroinflammation and Alzheimer’s disease-like pathology despite a 6-month recovery period in mice. Journal of Neuroinflammation. doi.org/10.1186/s12974-024-03290-6. To read the original article click here.

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Common Viruses May Be Triggering the Onset of Alzheimer’s Disease

AHA Publisher — Wed, 03 Aug 2022 07:00:09 +0000

Patrick Tims via NaturalHealth365 – Alzheimer’s disease can begin almost imperceptibly, often masquerading in the early months or years as forgetfulness that is common in older age. What causes the disease remains largely a mystery. But researchers at Tufts University and the University of Oxford, using a three-dimensional human tissue culture model mimicking the brain, have shown that varicella zoster virus (VZV), which commonly causes chickenpox and shingles, may activate herpes simplex (HSV), another common virus, to set in motion the early stages of Alzheimer’s disease. Normally HSV-1 – one of the main variants of the virus – lies dormant within the neurons of the brain, but when it is activated it leads to accumulation of tau and amyloid beta proteins, and loss of neuronal function—signature features found in patients with Alzheimer’s. “Our results suggest one pathway to Alzheimer’s disease, caused by a VZV infection which creates inflammatory triggers that awaken HSV in the brain,” said Dana Cairns, GBS12, a research associate in the Biomedical Engineering Department. “While we demonstrated a link between VZV and HSV-1 activation, it’s possible that other inflammatory events in the brain could also awaken HSV-1 and lead to Alzheimer’s disease.” The study is published in the Journal of Alzheimer’s Disease Viruses Lying in Wait “We have been working off a lot of established evidence that HSV has been linked to increased risk of Alzheimer’s disease in patients,” said David Kaplan, Stern Family Professor of Engineering and chair of the Department of Biomedical Engineering at Tufts’ School of Engineering. One of the first to hypothesize a connection between herpes virus and Alzheimer’s disease is Ruth Itzhaki of the University of Oxford, who collaborated with the Kaplan lab on this study. “We know there is a correlation between HSV-1 and Alzheimer’s disease, and some suggested involvement of VZV, but what we didn’t know is the sequence of events that the viruses create to set the disease in motion,” he said. “We think we now have evidence of those events.” According to the World Health Organization, an estimated 3.7 billion people under the age of 50 have been infected with HSV-1—the virus that causes oral herpes. In most cases it is asymptomatic, lying dormant within nerve cells. When activated, it can cause inflammation in nerves and skin, causing painful open sores and blisters. Most carriers—and that’s one in two Americans according to the CDC—will have between very mild to no symptoms before the virus becomes dormant. Varicella zoster virus is also extremely common, with about 95 percent of people having been infected before the age of 20. Many of those cases are expressed as chicken pox. VZV, which is a form of herpes virus, can also remain in the body, finding its way to nerve cells before then becoming dormant. Later in life, VZV can be reactivated to cause shingles, a disease characterized by blisters and nodules in the skin that form in a band-like pattern and can be very painful, lasting for weeks or even months. One in three people will eventually develop a case of shingles in their lifetime. The link between HSV-1 and Alzheimer’s disease only occurs when HSV-1 has been reactivated to cause sores, blisters, and other painful inflammatory conditions. How Sleeping Viruses May Wake To better understand the cause-and-effect relationship between the viruses and Alzheimer’s disease, the Tufts researchers re-created brain-like environments in small 6 millimeter-wide donut-shaped sponges made of silk protein and collagen. They populated the sponges with neural stem cells that grow and become functional neurons capable of passing signals to each other in a network, just as they do in the brain. Some of the stem cells also form glial cells, which are typically found in the brain and help keep the neurons alive and functioning. The researchers found that neurons grown in the brain tissue can be infected with VZV, but that alone did not lead to the formation of the signature Alzheimer’s proteins tau and beta-amyloid—the components of the tangled mess of fibers and plaques that form in Alzheimer’s patients’ brains—and that the neurons continued to function normally. However, if the neurons already harbored quiescent HSV-1, the exposure to VZV led to a reactivation of HSV, and a dramatic increase in tau and beta-amyloid proteins, and the neuronal signals begin to slow down. “It’s a one-two punch of two viruses that are very common and usually harmless, but the lab studies suggest that if a new exposure to VZV wakes up dormant HSV-1, they could cause trouble,” said Cairns. “It’s still possible that other infections and other pathways of cause and effect could lead to Alzheimer’s disease, and risk factors such as head trauma, obesity, or alcohol consumption suggest they may intersect at the re-emergence of HSV in the brain,” she added. The researchers observed that the VZV infected samples started to produce a higher level of cytokines—proteins which are often involved in triggering an inflammatory response. Kaplan noted that VZV is known in many clinical cases to cause inflammation in the brain, which could possibly lead to activation of dormant HSV and increased inflammation. Repeat cycles of HSV-1 activation can lead to more inflammation in the brain, production of plaques, and accumulation of neuronal and cognitive damage. A vaccine for VZV—to prevent chickenpox and shingles—has also been shown to considerably reduce the risk of dementia. It’s possible that the vaccine is helping to stop the cycle of viral reactivation, inflammation, and neuronal damage. The researchers also noted the long-term neurological effects that some COVID patients have experienced from the SARS-CoV-2 virus, particularly among the elderly, and that both VZV and HSV-1 can be reactivated after a COVID infection. Keeping an eye on possible follow-on cognitive effects and neurodegeneration would be advisable in these cases, they said. To read the original article click here.

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