Many of us believe that we are great drinkers and that alcohol does not affect us as much. People who are able to drink without showing any sign of inebriation are known as social drinkers. In short, they are not addicted to alcohol but will not turn down the opportunity to have a good time! While it may seem like it doesn’t affect you, new studies suggest that it is just an illusion, even if you have high tolerance, alcohol affects your cognitive and motor functions more than you think.

The study reveals the below implications and techniques:

• Researchers used a new MRI technique to precisely measure brain electrical activity.
• By comparing brain scans before and after drinking, scientists identified specific areas affected by alcohol and how much brain activity slowed down.
• Participants were chosen to be regular social drinkers without alcohol addiction, ensuring the study focused on the effects of alcohol alone.
• MRI technology provided reliable data on brain activity changes caused by alcohol consumption.

How does the brain react to alcohol?

Think of it as the foundation for your brain's performance. When brain conductivity is high, information flows smoothly, and that helps your brain in rapid processing and response. On the other hand, low conductivity can hinder cognitive function, leading to slower thinking, impaired memory, and difficulties with coordination.

A study conducted at the Neuroscience Research Australia (NeuRA) and UNSW Science unveiled a startling connection between alcohol consumption and brain conductivity.

What is the connection between alcohol consumption and brain activity?

While many people brush off the effects of alcohol as temporary changes in behaviour, the reality is much more complex. Beyond the obvious impacts on coordination and judgment, alcohol significantly alters brain function. Alcohol dramatically slowed down brain activity, especially in areas responsible for decision-making, planning, and physical coordination. This decline was so significant that it resembled the brain changes seen in normal ageing. This means even one drink could temporarily accelerate the ageing process of your brain.

Alcohol and Brain activity: What does the study Imply?

The implications of this research are far-reaching. It provides compelling evidence that alcohol consumption has a direct and measurable impact on brain function. The discovery that alcohol can significantly reduce brain conductivity opens new avenues for understanding the neurocognitive effects of alcohol abuse and dependence. While you may not feel like alcohol is affecting you and you have a high tolerance, it most definitely changes and affects your decision-making abilities and impulse control.

Furthermore, the MRI technique employed in the study could be a valuable tool for assessing the impact of other substances on the brain and for developing interventions to mitigate alcohol-related brain damage.

reaImagine developing a strange medical condition in which an injury or even a minor fall may trigger a process that may gradually turn muscles, tendons and ligaments into bone.

This is what fibrodysplasia ossificans progressiva (FOP), one of the world’s rarest genetic disorders, looks like.

The US Food and Drug Administration recently approved a new treatment option for FOP called Atebrioz (zilurgisertib), a once-daily pill developed by Mirum Pharmaceuticals.

Adults and children aged 12 years and above with FOP are eligible for this treatment. It is designed to reduce the formation of new bone outside the skeleton.

What Is Fibrodysplasia Ossificans Progressiva?

FOP is a rare genetic disease in which connective tissues like muscles, tendons and ligaments gradually turn into bone. The abnormal bone formation is known as heterotopic ossification, meaning bone starts to develop in places where it should not.

Over time, this can pose restriction in movement, cause deformities and lead to severe disability. The condition could affect quality of life significantly as well as shorten life expectancy.

FOP is usually diagnosed in childhood. According to Mirum, around 300 people in the US and about 900 worldwide are known to have the condition.

Also read: New RNA Therapy For ALS, The Disease Stephen Hawking Had: Patient With Rare Motor Neuron Disease Improves

Why Does The Body Starts Making Bone In The Wrong Places?

FOP is caused by mutations in a gene involved in bone growth, especially the ACVR1 gene, which produces a protein called activin A receptor type-1, or ALK2. In people with FOP, this pathway becomes abnormally active. As a result, the body can start producing bone within soft tissues.

This process can occur in episodes called flare-ups. Trauma, surgery or other triggers can sometimes provoke inflammation and subsequent abnormal bone formation. The problem is that once mature bone has formed in these tissues, it can permanently restrict movement.

Also read: Rare Pregnancy Infections Linked To 3-Fold Higher Autism Risk: What Is TORCH?

More About The New Drug

Atebrioz contains zilurgisertib, an oral drug that blocks ALK2, the protein that is abnormally active in most people with FOP and triggers bone formation outside the skeleton.

The aim is not to remove bone that has already formed. Instead, the treatment is designed to reduce the formation of new abnormal bone.

FDA’s approval was based on a randomised, placebo-controlled trial involving 63 people with FOP. Participants received either zilurgisertib or placebo for 24 weeks, followed by an extension period.

At week 24, patients receiving Atebrioz had an average 3.2 cm³ decrease in the volume of newly formed abnormal bone, compared to a 24.6 cm³ increase in the placebo group. The FDA said the difference supported the drug’s effectiveness in reducing new heterotopic ossification.

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Symptoms & Treatment Of FOP

The disease can vary between individuals, but abnormal bone formation can progressively restrict movement. People with FOP may develop difficulty moving their neck, shoulders, spine, hips and other joints as new bone forms around them.

The condition can eventually affect mobility substantially. Extra bone formation can also interfere with everyday activities and contribute to severe disability.

Another characteristic feature is that people with FOP are often born with abnormalities of the big toes, which can help doctors recognise the rare condition early.

Atebrioz is not the first FDA-approved treatment for FOP. The FDA approved Sohonos (palovarotene) in 2023 as the first treatment for the disease.

More recently, the FDA approved Pasatru (garetosmab-grts) in August 2026, making Atebrioz the third FDA-approved treatment for FOP. The newer options differ in how they target the abnormal bone formation.

A confirmed case of mpox has been detected in Bunia, the capital of Ituri province in the Democratic Republic of Congo (DRC), where health authorities are already battling the country's largest-ever Ebola outbreak.

The development has raised concerns about the additional pressure on an already stretched outbreak response and the overall healthcare system.

The mpox case was confirmed after a 21-year-old woman was hospitalised with skin lesions that ae commonly seen in mpox.

The two viruses are not associated with each other, but the threat of two highly infectious diseases is now being navigated in the same area at the same time.

Mpox Case In Congo Amid Ebola Outbreak

Ituri is at the centre of one of the worst Ebola outbreaks the country has ever seen. As of September 23, the DRC reported 7,890 confirmed Ebola cases and around 3,799 deaths. The a case-fatality ratio, according to WHO, stayed put at 48.1%. Ituri, the epicenter of the outbreak, solely accounted for 6,032 confirmed cases.

The Ebola outbreak has also expanded geographically, with new cases reported across 63 health zones in seven provinces. The WHO says the continued spread is increasing the risk of cross-border transmission.

The appearance of mpox in Bunia, against the backdrop of Ebola, creates another challenge for surveillance, testing, infection prevention and safety of healthcare workers.

Also read: 1,370 Mpox Cases, 7 Deaths Reported In July: WHO Says Risk Remains Moderate

What Is Mpox?

Mpox is a viral disease that can cause fever, swollen lymph nodes, muscle aches, and peculiar rash or skin lesions. It spreads mainly through close physical contact with an infected person.

Some people recover without complications, while others can develop serious symptoms, particularly those with weak immune systems.

The newly case is especially alarming as the DRC had declared an end to mpox as a national public health emergency in April, following a three-year outbreak that resulted in more than 34,000 confirmed cases nationwide.

Also read: Canada Confirms Clade 1 Strain of Mpox: Know How It Impacts Human

Burden On An Already Overwhelmed Healthcare System

The two diseases are caused by different viruses and spread differently. A confirmed mpox case does not indicate that Ebola has mutated or that the two outbreaks are connected.

The WHO says the Ebola response is already operating under difficult conditions, with conflict, insecurity, population displacement and limited access to basic services hampering surveillance, contact tracing, infection prevention and timely care.

The concern is that health systems, that were already dealing with a major outbreak, now have another infection to detect, investigate and contain.

Bunia is not just another location where a case has been detected. It is the capital of Ituri, where the Ebola outbreak is the most concentrated.

WHO teams have described Bunia as a key operational hub for the response, with flights transporting healthcare workers, medicines and other supplies to affected regions.

The immediate priority will be investigation, contact tracing, and surveillance to determine whether the case is linked to a wider cluster.

DRC is already conducting extensive contact monitoring for Ebola. As of September 23, more than 32,000 people were listed for follow-up, depicting the scale of the response.

The US Food and Drug Administration has approved tavapadon, a once-daily oral medicine for adults with Parkinson’s disease. This has added a new option to Parkinson's treatment strategy that has long relied on drugs that mimic the brain’s dopamine supply. The drug will be sold in the US under the brand name Juvmo.

Tavapadon is different from traditional dopamine agonists because it selectively targets D1 and D5 dopamine receptors. It has been studied both as an early treatment and alongside levodopa in people with more advanced Parkinson’s disease and motor fluctuations.

Parkinson’s Disease & Dopamine

Parkinson’s disease is a progressive neurological disorder in which dopamine-producing nerve cells in a region of the brain called the substantia nigra disappear gradually.

Dopamine is essential for controlling movement. As its levels fall, people can develop symptoms like tremor, stiffness, slowness of movement and problems with balance.

This is why many Parkinson’s treatments entail increasing dopamine levels or mimicking its effects in the brain.

How Does Tavapadon Work?

Also read: Parkinson’s Is Rising Across US, But Not Equally: Why Are Some States Seeing More Cases Than Others?

Tavapadon is a selective D1/D5 partial dopamine agonist. It means that it does not simply increase the amount of dopamine in the brain. Instead, it binds to particular dopamine receptors and partially activates them, essentially helping reproduce some of dopamine’s signalling effects.

Most currently available dopamine agonists target D2/D3 receptors. Tavapadon’s D1/D5 is therefore one of its distinguishing characteristics. Researchers have been investigating whether this drug can can help provide motor symptom relief while avoiding some adverse effects linked with dopamine receptor activation.

The FDA’s approval was supported by the phase 3 TEMPO clinical programme. In TEMPO-1, which involved 529 people with early Parkinson’s disease, both 5 mg and 15 mg daily doses of tavapadon significantly improved motor function compared to placebo after 26 weeks.

The drug has also been studied in people already taking levodopa who experience motor fluctuations, a common problem with progressive Parkinson’s. In the TEMPO-3 trial involving 507 participants, adding tavapadon to levodopa increased daily 'on' time without troublesome dyskinesia compared to placebo.

As Parkinson’s disease progresses, some people taking levodopa experience periods when the medicine is working well and movement improves. This is called 'on' time. When the medication’s effect wears off and Parkinson’s symptoms return, it is called 'off' time.

Treatment aims to increase 'on' time while limiting troublesome involuntary movements, known as dyskinesia.

Side Effects Of Tavapadon?

Tavapadon was generally tolerated in the clinical trials, but it is not free of side effects. In the TEMPO-1 trial, the most commonly reported adverse events were:

• Nausea
• Headache
• Dizziness

The FDA’s approval follows data showing improvement in Parkinson’s symptoms, but longer-term safety remains an important factor that needs more investigation.

Dopamine agonists can also be associated with sleepiness, low blood pressure on standing, hallucinations and impulse-control disorders. These issues remain relevant when doctors consider where tavapadon fits into an individual’s treatment plan.

Tavapadon treats the symptoms of Parkinson’s disease. It does not restore the dopamine-producing nerve cells that have been lost or stop the neurodegenerative process.