Observational studies of psychiatric diseases such as schizophrenia, bipolar disorder and major depression have long tied viral infections with behavioral symptoms in these disorders, but scientists have been unable to find direct evidence of suspected viruses in the brain. Experts say that’s possibly because viruses may not get directly inside the brain, but may target the brain lining instead.

After testing that idea using postmortem human brain samples and the electronic medical records of 285 million patients, a team of Johns Hopkins Medicine scientists says it has found such evidence in the form of the liver-damaging hepatitis C virus in the human brain’s choroid plexus, a collection of cells that make up the lining of the fluid-filled cavities, or ventricles, and — notably — produce the cerebrospinal fluid that protects the brain and spinal cord…

…’Our findings show that it’s possible that some people may be having psychiatric symptoms because they have an infection, and since the hepatitis C infection is treatable, it might be possible for this patient subset to be treated with antiviral drugs and not have to deal with psychiatric symptoms,’ Sabunciyan says.

The influence of the heart and circulatory system occurs within milliseconds, and every single heartbeat plays a role. The role of the heart in the psyche and cognition is evident in the high coincidence of cardiovascular diseases, such as high blood pressure and heart attack, and mental illnesses, such as depression and anxiety disorders.

There are a number of explanations for this high coincidence, but none of them have been definitively proven yet. For example, negative psychological reactions to a diagnosis of cardiovascular disease are cited as a reason for the development of mental illness. On the other hand, an unhealthy lifestyle in the presence of mental illness is considered a risk factor for the development of cardiovascular disease.

The concept is based on integrated brain–body states. Every physical process, such as a heartbeat or any change in blood pressure or metabolism, is automatically accompanied by a mental or psychological process. This means that the two are inextricably linked.

Staring at the ceiling while the clock blinks 3am doesn’t only sap energy for the next day. A large, long-running US study of older adults has now linked chronic insomnia to changes inside the brain that set the stage for dementia.

The researchers, from the Mayo Clinic in the US, followed 2,750 people aged 50 and over for an average of five and a half years. Every year the volunteers completed detailed memory tests and many also had brain scans that measured two telltale markers of future cognitive trouble: the buildup of amyloid plaques, and tiny spots of damage in the brain’s white matter – known as white-matter hyperintensities.

Participants were classed as having chronic insomnia if their medical records contained at least two insomnia diagnoses a month apart – a definition that captured 16 percent of the sample.

Even hearing the phrase “Huntington’s disease” will make a room suddenly somber. So the joy that accompanied a recent announcement of results of an experimental gene therapy for the deadly diseases signaled an unfamiliar sense of hope.

In a small clinical trial, brain injections of a virus that codes for a tiny segment of RNA may have prevented the formation of the rogue proteins that make Huntington’s so devastating. The early results, announced September 24 in a news release, show that over three years, the treatment slowed Huntington’s progression by up to 75 percent. While not a cure, the treatment could potentially give people living with Huntington’s disease, who might otherwise face early disability and death, the gift of many more years of life.

The International Advisory Committee on Clinical Trials led a multinational panel updating the McDonald criteria, adding the optic nerve as a fifth anatomical location and allowing specific magnetic resonance imaging (MRI) and cerebrospinal fluid (CSF) markers to support diagnosis without mandatory dissemination in time in defined scenarios.

Multiple sclerosis diagnosis has long required proof that lesions occur in different places and at different times, with MRI and CSF biomarkers gradually shortening time to treatment.

Previous revisions improved sensitivity and specificity across ages and regions, yet misdiagnosis risk still persists, especially with overlapping conditions and when access to specialized tests is limited.