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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The NHS will not be automatically inviting all men above a certain age to check for prostate cancer, unlike the approach for some other cancers. The UK National Screening Committee has suggested that the prostate-specific antigen (PSA) test should only be actively offered to men carrying the BRCA gene mutation, which increases their risk. Still, men can request a PSA test from their GP in certain situations.
Olympic cycling hero Sir Chris Hoy, who has received a terminal diagnosis, is among those campaigning for men with known risk factors to be invited for a PSA test at a certain age, even if they do not have any symptoms.
A prostate-specific antigen (PSA) test checks the level of PSA in your blood. PSA is a protein produced by the prostate, a small gland in the male reproductive system located just below the bladder. The prostate produces the fluid part of semen.
The NHS says the test might be suggested if you notice symptoms that could point to prostate cancer, such as:
However, for most men, urinary symptoms are caused by something other than cancer.
A PSA test is usually carried out at a hospital or GP surgery by a nurse or other healthcare professional. Men are asked to avoid certain activities for 48 hours before the test, as these can temporarily raise PSA levels and affect the result. Activities to avoid include anything that leaves you out of breath, like strenuous exercise.
If a man’s PSA level comes back high, they may be offered a repeat test to see if the levels remain raised. If they do, the GP may refer them to a specialist for further investigations, such as a biopsy or an MRI scan.
PSA levels can rise for many reasons, including minor infections, and around 75% of men with a raised PSA do not have prostate cancer. A high reading can lead to referrals for unnecessary biopsies or MRI scans, or treatment for tumours that might never have caused harm.
The PSA test can also miss aggressive cancers. Research has shown that roughly 15% of men with a normal PSA result may actually have prostate cancer.
Routine PSA testing is not offered as standard on the NHS. You might be offered a test if a doctor suspects symptoms that could indicate prostate cancer. Men undergoing treatment for a prostate condition may be offered regular PSA checks to monitor how treatment is progressing.
Men aged 50 and over can request a PSA test from their GP, even without symptoms. Campaigners say many men are unaware that they are at higher risk of prostate cancer and should be actively encouraged to think about having a PSA check.
If the UK National Screening Committee’s recommendation is approved by the Government next year, men with the BRCA gene mutation could also be invited for a PSA test. Men who think a family member might have had the BRCA gene mutation can request a genetic test on the NHS to find out.
(Credit-Canva)
Usually, when your muscle hurts, it's just from working out too hard, pulling a muscle, or getting a bruise. The pain is normal and goes away after a while. However, the National Health Service (NHS) wants people to know that some types of muscle pain are not normal and could be a medical emergency.
Muscle cramps and pain are considered normal; you may have hurt your leg by a fall, stretched your muscles wrong etc. However, not all pain is harmless and it can lead to more serious consequences. Here is how you identify whether your muscle pain is in dangerous territory or not.
NHS explains that one should get help right away if your muscle pain feels like:
It's a major red flag if this pain gets much worse when you try to move the sore body part. If you have these symptoms, doctors worry it could be a serious problem called Compartment Syndrome.
The strong, thin layer of tissue which holds your muscles is called fascia. A compartment is just one of these tight bundles of muscle, blood vessels, and nerves.
Compartment syndrome happens when something causes a lot of swelling or bleeding inside that bundle. Because the fascia around the muscle doesn't stretch easily, the pressure inside the compartment goes up very fast.
This high pressure squeezes the blood vessels and nerves, stopping blood from flowing properly. When blood can't get in to bring oxygen or out to remove waste, the muscle tissue starts to die. That's what causes the severe pain.
It's important to watch out for these symptoms, especially if they follow an injury or intense activity:
Intense Pain: The pain is severe, much worse than normal soreness. It might feel like a deep, burning ache inside the muscle.
Worse with Movement: If you try to move the sore arm or leg, the pain gets instantly and much worse.
Swelling: The muscle might look puffy, or it might feel rock-hard or tight to the touch.
Odd Sensations: You might feel numbness, a pins-and-needles feeling, or feel weak in your hand or foot.
Tightness: The area feels so tight you have trouble moving it normally.
If the problem is sudden and severe (Acute Compartment Syndrome), it is an emergency, and doctors must act right away.
The surgeon makes a long cut through the tough skin (the muscle cover) that is squeezing the muscle. This immediately releases the pressure, allowing blood to flow normally again to the muscle and nerves.
Afterward, you'll need pain medication, and sometimes a skin graft (taking skin from another part of your body) to cover the large wound. You will also need physiotherapy to help the muscle get back its full movement and strength. Since the pain here is linked to exercise, treatment usually starts with changes to your routine:

(Credit-Canva)
Researchers found how a cell’s energy source could affect depression and anxiety. The new study published in JNeurosci, led by Southern Medical University, was done on male mice. Researchers discovered that the adenosine triphosphate (ATP), which is the cell’s main energy source and a vital chemical messenger that helps communication between neurons, plays a part in depression and anxiety.
Because good brain cell communication is vital for controlling feelings, the study focused on the hippocampus, a brain area linked to memory, stress, and feeling depressed.
For years, scientists have looked for reasons behind mental health issues like depression and anxiety. While we may know that mental health disorders are caused due to different reasons, researchers have looked into how depression and anxiety stressors are communicated to the brain.
Mental health disorders do not have a single cause. According to the UK Mind organization, there are many different factors that can cause depression or trigger it. Things like childhood depression, life events, physical health problems, family history. So, understanding how this changes in mood and heightened emotions are communicated to the brain, could help us learn more about the root causes of depression as well.
Researchers studied what happened to ATP in the hippocampus when mice were under stress. They found that male mice who became more anxious or depressed after long-term stress also had lower levels of ATP.
These mice also had less of a key protein called connexin 43 (Cx43). Think of Cx43 as a tiny door that lets ATP out of cells so it can be used for communication. When Cx43 is low, ATP can't be released properly.
To prove that low ATP release was the problem, researchers did two things:
They lowered Cx43 (the "door") in healthy mice that hadn't been stressed. Even without stress, lowering Cx43 caused the mice to act depressed and anxious, and their ATP levels dropped. This showed that just blocking the ATP release was enough to cause mood problems.
They put Cx43 back (fixed the "door") in the stressed, depressed mice. When they did this, the ATP levels went back up, and the mice's anxious and depressed behaviors got much better.
The lead researcher, Gao, explained that this is the first time scientists have shown that low ATP release in the hippocampus drives both depression and anxiety—suggesting they share one single biological cause.
This is important because depression and anxiety often happen together and are hard to treat at the same time. The study suggests that future treatments could focus on improving ATP signaling by fixing or opening the Cx43 "door," potentially helping people with both conditions at once. The team plans to study female mice next to see if the same process happens in both sexes. Researchers mentioned how these finding can lead to better treatment options for people who have depression and anxiety. More focused studies will also help reveal how mental health issues are different in men and women, as they expand the research across sexes.
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