Cold sores are a common and often frustrating skin issue. While they may look like harmless blisters, cold sores are actually caused by the herpes simplex virus (HSV).

What Causes Cold Sores?

Cold sores are caused by the herpes simplex virus (HSV), which comes in two types: HSV-1 and HSV-2.

HSV-1 is the primary cause of cold sores, usually appearing around the mouth.

HSV-2 generally causes genital herpes but can also lead to cold sores.

While the appearance of cold sores caused by both HSV-1 and HSV-2 can look similar, their locations tend to differ. However, it is possible for HSV-1 to cause sores on the genitals and for HSV-2 to appear on the mouth.

How Do Cold Sores Spread?

Cold sores are highly contagious and can spread easily. The virus can be passed on through:

• Kissing or skin contact
• Sharing food, drinks, or cosmetics (such as lip balm)
• Oral sex, which can spread both cold sores and genital herpes

Even when a cold sore isn’t visible, the virus can still be spread through close contact. This makes prevention and management key to reducing outbreaks and the risk of infecting others.

Once someone contracts HSV, it stays in the body for life. While the virus remains dormant most of the time, it can reactivate and cause new sores, especially during periods of:

• Stress
• Illness
• A weakened immune system

Unfortunately, there’s no cure for the herpes virus, but the symptoms can be managed.

Symptoms of Cold Sores

Cold sores don’t just appear out of nowhere. Before the sore is visible, you may notice a tingling or burning sensation around the lips or face, which can occur several days before the sore forms. This is the best time to begin treatment to shorten the outbreak.

When a cold sore does appear, it often looks like a red, raised blister filled with fluid. The blister can be painful to touch, and there may be more than one. Cold sores usually last around two weeks and are contagious until they crust over and heal.

The Five Stages of a Cold Sore

Cold sores go through distinct stages as they develop and heal:

• Tingling and itching: You may feel these symptoms about 24 hours before the blister appears.
• Blisters: Small, fluid-filled blisters form, typically around the mouth.
• Bursting: The blisters burst and form painful sores.
• Scabbing: The sores dry out, scab over, and may itch or crack.
• Healing: The scab falls off, and the cold sore heals.

Risk Factors for Cold Sores

Certain factors can trigger the reactivation of HSV, leading to cold sores. These include:

• Infection, fever, or cold
• Sun exposure
• Stress
• Menstruation
• Dental work or injury
• Weakened immune system due to conditions like HIV/AIDS, eczema, or chemotherapy

Managing and Treating Cold Sores

There’s no cure for cold sores, but several treatments can ease the symptoms and help manage outbreaks.

Topical Ointments and Creams

Over-the-counter antiviral creams like docosanol (Abreva) or prescription ointments like penciclovir (Denavir) can help reduce the duration of an outbreak, especially if applied at the first sign of a cold sore.

Oral Medications

Prescription antiviral medications like acyclovir, valacyclovir, and famciclovir can also help, particularly for people who have frequent or severe outbreaks. Your doctor may recommend taking these medications regularly to prevent future outbreaks.

Home Remedies

There are also some home remedies that may provide relief, such as:

• Applying ice or a cold washcloth to the sore
• Using aloe vera gel or lemon balm lip balms
• Applying petroleum jelly to ease discomfort

Canker Sores vs. Cold Sores: What's the Difference?

While cold sores and canker sores may seem similar, they are quite different:

Cold sores are caused by the herpes virus, appear around the mouth, and are contagious.

Canker sores are not contagious and appear as ulcers inside the mouth or throat.

Preventing the Spread of Cold Sores

To avoid spreading cold sores:

• Wash your hands frequently
• Avoid close contact with others during an outbreak
• Don’t share food, drinks, or personal items like lip balm

Cold sores can be a persistent issue, but with proper care and management, you can reduce the frequency of outbreaks and prevent spreading the virus to others.

Smoking, diabetes, high blood pressure, high cholesterol, and obesity have always been recognized as major risk factors for heart disease.

New research has emerged saying these preventable conditions may do more harm than simply contribute to plaque buildup in the arteries. They may also encourage the formation of the most dangerous type of plaque, the kind that is most likely to rupture and trigger a massive heart attack.

The findings, presented at the European Society of Cardiology (ESC) Congress 2026, show that people with a greater number of modifiable cardiovascular risk factors were more likely to have widespread coronary plaque.

They may also have unstable and vulnerable plaques that can suddenly rupture, disrupting blood flow to the heart.

More Risk Factors = More Dangerous Plaques

Researchers analyzed coronary artery imaging data to understand how both modifiable and non-modifiable cardiovascular risk factors affect the characteristics of plaque.

The study found that patients with a higher burden of modifiable risk factors had plaques distributed across all three major coronary arteries.

More importantly, these individuals were more likely to develop lipid-rich plaques with thin fibrous caps, a trait of vulnerable plaques that are more likely to rupture.

On the other hand, people whose risk profile was dominated by non-modifiable factors, such as age or genetics, tended to have more stable plaque types.

"Our findings suggest that modifiable cardiovascular risk factors are associated not only with a greater amount of coronary plaque but also with more vulnerable plaque characteristics that are linked to future heart attacks," the researchers said.

Also read: ICMR Study Highlights India’s Silent Cholesterol Crisis: 9 In 10 Adults Have At Least One Abnormal Blood Lipid

Why Vulnerable Plaque Is Especially Dangerous?

Some plaques gradually harden and remain relatively stable for years, causing slow narrowing of the arteries. Others contain large amounts of fat covered by a very thin protective layer known as a fibrous cap.

These unstable plaques can rupture unexpectedly, prompting blood clots to form and suddenly block an artery, leading to a heart attack or stroke.

According to the researchers, individuals with multiple preventable cardiovascular risk factors were significantly more likely to have these high-risk plaques.

Also read: Risks Of Plastic Pollution: Study Finds Microplastics In Heart Arteries Can Cause Severe Heart Attacks

Smoking, Diabetes And high Blood Pressure Pose High Risk

Smoking chronically damages the inner lining of blood vessels, making it easier for cholesterol deposits to accumulate while also promoting inflammation and blood clot formation.

High blood pressure places constant stress on artery walls, accelerating plaque development and increasing the likelihood of rupture.

When several of these risk factors occur together, their harmful effects can compound, increasing both the quantity of plaque and likelihood to rupture.

Also read: Vapers & Smokers Have Equally Poor Physical Fitness & Blood Vessel Health, Study Finds

What Is Atherosclerosis?

Atherosclerosis is a chronic condition in which fatty deposits made up of cholesterol, inflammatory cells, calcium, and other substances accumulate inside artery walls.

Over time, these deposits narrow the arteries and reduce blood flow to vital organs. The condition often develops silently over decades before causing symptoms.

If a plaque ruptures, a blood clot can rapidly block blood flow, resulting in a heart attack or stroke. Smoking, diabetes, high blood pressure, obesity, and elevated LDL ("bad") cholesterol are among its leading preventable causes.

The researchers said the study highlights the importance of early identification and management of modifiable cardiovascular risk factors through smoking cessation, blood pressure control, diabetes management, cholesterol-lowering treatment, regular physical activity, a healthy diet, and maintaining a healthy weight.

Sleep disturbances are among the most debilitating symptoms of Alzheimer’s disease. It often appears years before significant memory decline and other symptoms.

A new study from researchers at the University of Kentucky suggests that this sleep loss may not be permanent.

Instead, it could be driven by an immune response in the brain that may be reversible, sparking hope for new treatments.

Published in the journal Alzheimer’s & Dementia, the study found that brain immune cells called microglia, rather than amyloid plaques themselves, are the primary cause of sleep disruption in Alzheimer’s disease.

In mouse-based trials, researchers were able to restore more than two hours of sleep per day by temporarily removing these immune cells, without reducing amyloid plaques.

Can Sleep Be Restored In Alzheimer’s Patients?

For years, scientists believed that sleep problems in Alzheimer’s were caused by the accumulation of amyloid plaques or the gradual death of brain cells. However, this study points in a different direction.

Researchers discovered that when amyloid plaques begin forming in the brain, they activate microglia, the brain’s resident immune cells.

Instead of protecting the brain, these cells cause inflammation that keeps brain circuits active, preventing sleep.

Using a drug called pexidartinib (PLX3397), the researchers temporarily depleted around 87% of microglia in Alzheimer’s mouse models.

This restored over two hours of daily sleep, particularly non-rapid eye movement (NREM) sleep, which is essential for tissue repair, memory strengthening, and clearing waste products from the brain.

Notably, the improvement occurred without changing amyloid plaque levels, suggesting that inflammation is manageable.

Also read: Captain ‘Sully’ Sullenberger, ‘Miracle On The Hudson’ Pilot, Reveals Early-Stage Alzheimer’s Diagnosis

'Paradigm Shifting' Findings

Lead researcher Dr. Shannon L. Macauley, associate professor of physiology at the University of Kentucky College of Medicine, said, “Basically, we showed that it is not the plaques themselves, or solely dysfunctional neurons, that cause sleep loss but actually microglia.

Microglia are immune cells that, when they respond to plaques, kick off this elaborate cascade of inflammation, as if the microglia are partying all night, and keeping the brain awake.”

She also highlighted why losing restorative sleep can accelerate disease progression.

“That restorative sleep is super important for physical repair, learning and memory and washing out the toxins of the day. When Alzheimer’s patients lose this stage, they lose their brain’s primary cleaning cycle, creating a feed-forward loop that may drive further damage,” she explained.

First author Dr. Nicholas J. Constantino said one of the biggest surprises was that sleep problems did not worsen as amyloid plaques increased.

“I expected that as plaque burden became more severe, sleep disruption would also worsen. The disruptions in sleep… did not worsen by 18 months, despite more than double the amount of plaque burden,” Constantino said.

Also read: What Is Type 3 Diabetes? Insulin Resistance In The Brain That Could Trigger Alzheimer’s

Why Do Alzheimer’s Patients Lose Sleep?

Poor sleep and Alzheimer’s create a vicious cycle. Sleep deprivation reduces the brain’s ability to clear amyloid-beta and tau proteins, which can accelerate disease progression, while worsening sleep.

Sleep disturbances affect up to half of people living with Alzheimer’s disease. The disease disrupts sleep due to various reasons:

Overactive microglia: As shown in the new study, immune cells become chronically activated by amyloid plaques, releasing inflammatory signals that keep the brain in a heightened state of activity.

Damage to sleep-regulating brain regions: Alzheimer’s progressively affects areas like the hypothalamus and brainstem that regulate the sleep-wake cycle.

Loss of NREM sleep: Due to lack of deep sleep, the brain’s ability to clear metabolic waste, including amyloid plagues weakens.

Circadian rhythm disruption: Degeneration of the brain’s internal clock leads to broken sleep and daytime drowsiness. This fuels confusion and agitation associated with the disease.

Obesity has always been considered as one of the contributors to heart disease, diabetes, and stroke.

Now, growing research suggests that excess body fat, particularly in your 40s and 50s, may also accelerate brain aging and raise the risk of long-term cognitive decline.

Researchers say that obesity is not just linked with memory problems but also to significant changes in the brain structure.

Maintaining a healthy weight, especially during midlife, could help prevent memory problems and overall cognitive decline.

Higher BMI Linked To Faster Brain Aging

A recent study by researchers at the University of Georgia followed more than 8,200 adults aged 50 years and older for nearly 24 years.

The researchers found that individuals whose body mass index (BMI) increased over time experienced faster declines in cognitive performance than it would with normal aging. Excess body weight affected several aspects of cognition, including memory, planning, decision-making, problem-solving, emotional regulation, and concentration.

Lead author Dr. Claire Sexton (University of Georgia College of Public Health) said, "Maintaining a healthy body weight throughout adulthood may be an important strategy for preserving cognitive health later in life."

The study adds to the evidence that preventing weight gain throughout adulthood could become crucial for reducing dementia risk.

Also read: Grade-1 Fatty Liver: More Indians Are Developing It at Lower BMIs. What's Behind the Shift?

How Does Obesity Affect The Brain?

Chronic Inflammation

Obesity causes chronic low-grade inflammation, which can potentially damaging neurons essential for learning and memory.

Insulin Resistance

The brain relies on glucose for energy. Insulin resistance, common in obesity, may impair how brain cells use glucose, affecting memory and thinking.

Reduced Blood Flow

Obesity increases the risk of hypertension, atherosclerosis and vascular disease, reducing blood supply to brain tissue and potentially accelerating cognitive decline.

Visceral Fat

Experts believe visceral fat, the fat surrounding internal organs, may be more damaging than body weight alone. It produces inflammatory chemicals linked to brain changes and dementia risk.

Also read: Beyond Weight Loss: Scientists Discover How Exercise Can Help Reverse Muscle Aging

Growing Evidence

The latest findings are supported by several years of research. A large review published in Practical Neurology concluded that obesity is associated with smaller hippocampal volume, temporal lobe atrophy, mild cognitive impairment and increased Alzheimer's disease risk.

Some studies have suggested that obesity during midlife may nearly double the risk of developing Alzheimer's disease or dementia later in life.

Another review on obesity and aging reported that higher BMI is associated with poorer verbal memory, slower information processing and reduced executive function, particularly among older adults.

In January 2026, researchers also used genetic analyses to suggest that obesity and high blood pressure may directly contribute to dementia.

Can The Risk Be Reduced?

With a few lifestyle improvements, overweight and obese individuals can maintain a healthy BMI, reducing the risk of faster brain ageing and cognitive degradation. Experts recommend focusing on overall metabolic health rather than the number on the weighing scale alone.

Maintaining a healthy weight, regular exercise, controlling blood pressure, cholesterol and diabetes, following a Mediterranean diet, getting adequate sleep, remaining socially and mentally active can help maintain a healthy body weight.