The COVID-19 pandemic may be over, but our immune systems are still feeling the impact. After years of battling constant viral threats, from COVID-19 to seasonal flu and other infections, our body’s defense system is exhausted. Many people continue to experience lingering inflammation, frequent illnesses, and slower recovery times. This extended state of immune stress has compromised us further to chronic illness, including autoimmune diseases and even neurodegenerative diseases such as Parkinson's. So why is our immune system still in trouble? And how do we give it its power back? Understanding immune exhaustion is the beginning of rebuilding our body's natural immunity.
A weakened immune system makes people more susceptible to disease, mental illnesses, and even sleep disorders. Now, new research indicates that immune system depletion may play an important role in the onset of Parkinson's disease, a degenerative neurologic disorder that compromises movement and cognition.
Dysfunctional immune response is a leading cause of long-standing inflammation within the body, that has been found to contribute towards a multitude of conditions, including cardiovascular conditions, diabetes, depression, and neurodegenerative diseases such as Alzheimer's.
As people age, their immune system naturally becomes less effective. This deterioration, referred to as immune exhaustion, may be a key contributor to the onset and progression of Parkinson’s disease. Rebecca Wallings, a Parkinson’s Foundation Launch Award grant recipient and senior postdoctoral fellow at the University of Florida, believes that an accumulation of exhausted immune cells could be driving neurodegeneration in Parkinson’s patients.
Parkinson's disease is most commonly linked with the degeneration and loss of dopaminergic neurons—motor nerve cells that produce dopamine, an essential neurotransmitter for movement. While researchers have long suspected inflammation is involved in this neurodegeneration, the mechanisms are not yet well understood.
Wallings' study is on immune cell exhaustion, a process by which aging immune cells fail to control immune responses effectively. Her research indicates that instead of dampening inflammation in Parkinson's patients, attempts should be made to rejuvenate the immune system to regain its functionality.
One of the major findings of Wallings' work is the function of mitochondrial impairment in immune cell exhaustion. Mitochondria are commonly called the powerhouses of cells, as they are vital for generating energy. As mitochondria age and become inefficient, immune cells fail to function well, potentially accelerating neurodegeneration in Parkinson's disease.
Wallings has found that mutations in the LRRK2 gene, a recognized genetic risk factor for Parkinson's disease, are linked with defective mitochondrial function and immune cell exhaustion. Her current work includes testing various therapeutic approaches to restore mitochondrial function in immune cells with the potential to enhance the immune system and potentially prevent or treat Parkinson's disease.
For decades, the standard practice in treating Parkinson's has been to suppress brain inflammation. Yet Wallings' work indicates that instead of slowing down immune responses, restoring the immune system could be a more successful strategy. By addressing mitochondrial impairment and immune resilience, researchers can potentially reverse or slow down Parkinson's disease.
Wallings is now looking into how to rejuvenate immune cells by fixing mitochondria. She studies immune cells from patients with Parkinson's as well as from healthy subjects and performs experiments on animal models to determine if rejuvenation of the immune system could result in improved disease outcomes.
While there is no cure for Parkinson's disease, some lifestyle adjustments may decrease the chances of developing the illness. Since neurodegenerative diseases are associated with chronic inflammation and immune dysfunction, developing habits that enhance immune function might prove helpful.
Diet: There is evidence to suggest that eating in accordance with the Mediterranean or MIND diets, both high in antioxidants, healthy fats, and anti-inflammatory foods, can encourage brain wellness and reduce Parkinson's risk.
Avoiding Dangerous Substances: Restricting alcohol and nicotine use can maintain a robust immune system and suppress inflammation.
Reducing Stress: Chronic stress weakens immune function, so methods such as meditation, exercise, and sufficient sleep can lead to improved overall well-being.
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An international team of researchers has developed an artificial intelligence (AI)-based tool that can significantly improve care for glaucoma -- a leading cause of irreversible blindness worldwide, according to a study published in The Lancet Primary Care journal today.
Researchers led by those from the University of Lisbon in Portugal found that the AI-based screening tool halved the number of unnecessary referrals for glaucoma.
The study, released during the Glaucoma Awareness Week, also showed an accuracy level at par with human eye doctors.
"The high accuracy at excluding people without glaucoma is especially important, as false alarms can lead to unnecessary hospital visits, patient anxiety, and added strain on healthcare services," the researchers said.
According to the researchers, AI-based screening could:
The study was carried out at a single screening center in Lisbon, Portugal, in 2023.
The experts screened 671 adults aged 55-65 for glaucoma via the AI tool, analyzing images of the eyes. The images were then independently graded by six glaucoma experts.
The AI-tool:
While modelling studies suggest that screening could substantially reduce glaucoma-related visual impairment and blindness, barriers include the need for specialised diagnostic equipment and trained personnel, particularly in low- and middle-income countries, and the intrinsically low positive predictive value of screening tests.
In such a scenario, the new study showed that "AI may provide a more viable option than population-wide screening", which may seem impractical.
Glaucoma is a chronic disease that affects an estimated 80 million individuals globally, according to the World Glaucoma Association.
It is a progressive, degenerative disorder of the optic nerve that produces characteristic visual field damage.
The disease stems from a long asymptomatic phase, resulting in substantial underdiagnosis and delayed treatment.
Even in high-income countries, up to 50 percent of individuals with glaucoma remain undiagnosed, frequently presenting moderate to advanced disease at first detection.
By the year 2040, it is estimated that there will be 22 million individuals worldwide who are blind from glaucoma.
When to see a doctor for glaucoma:
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In adults, long periods of sleep deprivation has been linked to problems such as weakened immunity, weight gain, depression, and an increased risk of dementia. However, scientists are now paying closer attention to how sleep affects the brain much earlier in life.
However, a new University of North Carolina School of Medicine study suggests that disrupted sleep during early childhood may interfere with key stages of brain development and asl well as increase the risk of developing autism.
Sleep plays a crucial role in helping these synapses form and strengthen. During sleep, the brain organizes and stabilizes these neural connections, shaping the foundation for future brain function. If sleep is repeatedly disrupted during this delicate stage of development, the process may be affected.
Frequent waking or sleep disturbances could interfere with how these neural connections are formed, potentially influencing behavior and cognitive abilities later in life.
“The unique effects of sleep loss during development are largely unexplored,” Diering said. “Our data show that babies and children are more vulnerable to the negative effects of sleep disruption. We also found that sleep loss during this crucial period of time can negatively interact with underlying genetic risk for autism spectrum disorder.”
Sleep problems are already known to be common in people with autism. In fact, sleep disruption has been reported in more than 80 percent of individuals with autism spectrum disorder. However, researchers have long debated whether these sleep issues are a cause of the disorder or a consequence of it. Understanding how sleep interacts with brain development could help scientists detect autism earlier and potentially develop new treatment strategies.
In earlier work conducted in 2022, researchers examined how sleep disruption during early life might interact with genetic factors linked to autism. Using mouse models, they disrupted sleep during the third week of life, a developmental stage roughly comparable to ages one to two in humans.
The study found that sleep disruption during this period produced long lasting behavioral changes. Male mice that were genetically vulnerable to autism showed deficits in social behavior later in life. These results suggested that sleep disruption during critical stages of development may interact with genetic risk factors in ways that shape long term behavior.
To investigate further, researchers studied how developing and adult mice respond differently to sleep deprivation.
Using specially designed housing systems equipped with sensitive sensors, scientists tracked the animals’ breathing and movement. This allowed them to determine when the mice were awake and when they were asleep.
The researchers observed that adult mice were able to compensate for lost sleep. After experiencing sleep deprivation, the adults increased their sleep later during their normal active period. This process, known as sleep rebound, allowed them to recover some of the lost rest.
Younger mice behaved very differently. They showed no sleep rebound at all, meaning they did not compensate for the sleep they had lost. This finding suggests that younger brains may be far more vulnerable to the effects of sleep disruption.
The consequences were also visible in cognitive performance. Sleep deprived young mice performed poorly on learning and memory tasks, while adult mice were significantly more resilient after losing sleep.
The results showed that sleep deprivation in young mice significantly altered the formation of synapses. These changes were not seen in adult mice. “This now provides one of the largest and most comprehensive datasets to examine the molecular effects of sleep loss across the lifespan,” Diering said.
“Development is not something that one can go back and do again,” Diering said. “Sleep is important for the entire life and especially during development. Understanding what we know now will place greater emphasis on understanding sleep issues in ASD and could lead to an important therapeutic avenue to treat ASD and other developmental conditions.”
The findings highlight an important message for parents and caregivers. During early childhood, healthy sleep patterns may play a critical role in shaping the brain for years to come.
Credits: Canva
Using amphetamines, cocaine and cannabis can significantly increase your risk of having a brain stroke particularly among younger adults, according to a new University of Cambridge analysis
The findings highlight how recreational drug use may contribute to a preventable health risk, especially among people under the age of 55.
Megan Ritson, a stroke genetics researcher at the University of Cambridge and lead author said the results provide strong evidence linking certain drugs to stroke risk.
“These findings provide compelling evidence that drugs like cocaine, amphetamines, and cannabis are causal risk factors for stroke,” Ritson noted.
A stroke occurs when blood flow to part of the brain is interrupted. This can happen when a blood vessel becomes blocked by a clot, known as an ischemic stroke, or when a blood vessel bursts and causes bleeding in the brain, known as a hemorrhagic stroke. Both types can lead to serious brain damage and can be life threatening.
When researchers combined data from eight previous studies, they found that recreational amphetamine use was associated with more than double the risk of stroke across all adult age groups. For individuals under the age of 55, the increase was even greater. In this group, amphetamine use was linked to nearly triple the risk of stroke compared with people who do not use the drug.
Across all age groups, the analysis found that amphetamine use increased the risk of ischemic stroke by 137 percent and hemorrhagic stroke by 183 percent. These figures reflect relative risk, meaning the probability of stroke is higher among users compared with non users.
The analysis showed that cocaine use nearly doubled the risk of stroke of any kind and more than doubled the risk of hemorrhagic stroke. Additional genetic investigations were conducted alongside the main analysis to better understand whether the relationship might be causal rather than simply linked to other lifestyle factors.
Eric Harshfield, a genetic epidemiologist at the University of Cambridge, said the findings suggest the drugs themselves may play a direct role. “Our analysis suggests that it is these drugs themselves that increase the risk of stroke, not just other lifestyle factors among users,” Harshfield said.
Among people under the age of 55, cannabis use was linked to a 14 percent increase in stroke risk. Although the increase is lower than that associated with stimulant drugs, researchers say it remains important because cannabis is widely used.
The researchers also note that many of the studies included in the analysis relied on participants reporting their own drug use. Because of this, other lifestyle factors could potentially influence the results. Further research will be needed to better understand the biological mechanisms involved and how different patterns of drug use may affect stroke risk. Still, scientists say the evidence now available provides an important foundation for future public health strategies.
“These findings give us stronger evidence to guide future research and public health strategies,” Ritson said.
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