Pile of proteins in neurons found to cause Alzheimer’s

A team of Japanese researchers has identified how proteins collect abnormally in neurons which is a feature of neurodegenerative diseases like Alzheimer’s. Diseases such as Alzheimer's and Amyotrophic Lateral Sclerosis (ALS) are known to be accompanied by an abnormal build-up of proteins in neurons.

However, the trigger behind this accumulation remains unknown, according to the study that appeared in the journal eLife. The team, led by Associate Professor Kanae Ando of Tokyo Metropolitan University, focused on the presence of mitochondria in axons, the long tendril-like appendages that stretch out of neurons and form the necessary connections that allow signals to be transmitted inside our brains.

It is known that the levels of mitochondria in axons can drop with age, and during the progress of neurodegenerative diseases. The team used fruit flies to show that depletion of mitochondria in axons can directly lead to protein accumulation.

At the same time, significantly high amounts of a specific protein were found. Restoring the levels to normal led to a recovery in protein recycling. Such findings promise new treatments for neurodegenerative diseases, said researchers

“As populations age and the prevalence of neurodegenerative conditions continues to increase, the team’s findings present a vital step in developing therapies to combat these serious illnesses,” the study noted.

Diabetes impacts Alzheimer’s

Diabetes and Alzheimer's are two of the fastest-growing health concerns globally. Diabetes alters the body's ability to turn food into energy and affects an estimated one in 10 US adults. Alzheimer’s is among the top 10 leading causes of death in the US, according to the study. The researchers investigated how diet might affect the development of Alzheimer's in people with diabetes. They discovered that a high-fat diet reduces the expression of a specific protein in the gut called Jak3.

Mice without this protein showed a chain of inflammation from the intestine to the liver and then to the brain. As a result, the mice displayed Alzheimer's-like symptoms in the brain, along with cognitive impairment.

The researchers believe that the pathway from the gut to the brain involves the liver.

An Indian-origin scientist in his research has found that reducing the risk of dementia in Alzheimer's is possible by keeping diabetes well controlled or avoiding it in the first place. Narendra Kumar, an associate professor at the US-based Texas A&M University, who led the study published in the journal 'American Society for Biochemistry and Molecular Biology', found that diabetes and Alzheimer's disease are strongly linked.

"By taking preventative or amelioration measures for diabetes, we can prevent or at least significantly slow down the progression of the symptoms of dementia in Alzheimer's disease," he said.

Cadaver-derived hormone link

In a first, a team of British scientists has identified five cases of Alzheimer’s disease that are believed to have arisen as a result of medical treatments decades earlier, and are now banned.

Alzheimer’s disease is caused by the amyloid-beta protein, and is usually a sporadic condition of late adult life, or more rarely an inherited condition that occurs due to a faulty gene. According to the team from the University College London (UCL), UK, the five people acquired Alzheimer’s disease due to transmission of the amyloid-beta protein. In the paper, published in the journal Nature Medicine, the team described that they were all treated as children with a type of human growth hormone extracted from pituitary glands from deceased individuals (cadaver-derived human growth hormone or c-hGH). This was used to treat at least 1,848 people in the UK between 1959 and 1985, and used for various causes of short stature.

It was withdrawn in 1985 after it was recognised that some c-hGH batches were contaminated with prions (infectious proteins) which had caused Creutzfeldt-Jakob disease (CJD) in some people. c-hGH was then replaced with synthetic growth hormone that did not carry the risk of transmitting CJD. “There is no suggestion whatsoever that Alzheimer’s disease can be transmitted between individuals during activities of daily life or routine medical care," said lead author Professor John Collinge, Director of the UCL Institute of Prion Diseases.

"The patients we have described were given a specific and long-discontinued medical treatment which involved injecting patients with material now known to have been contaminated with disease-related proteins," he added.

The researchers previously reported that some patients with CJD due to c-hGH treatment (called iatrogenic CJD) also had prematurely developed deposits of the amyloid-beta protein in their brains. They suggested that individuals exposed to contaminated c-hGH, who did not succumb to CJD and lived longer, might eventually develop Alzheimer’s disease.