Study sheds new light on early stage alzheimer's disease


Study sheds new light on early stage alzheimer's disease

New light has been shed on how neuronal metabolism relates to the development of Alzheimer's disease in a recent study.

The research was conducted by scientists from Karolinska Institutet in Sweden and was published in the journal Proceedings of the National Academy of Sciences (PNAS).

Scientists have known that the disrupted metabolism of sugar, fat, and calcium is part of the process that results in the death of neurons in Alzheimer's disease.

However, for the first time, the experts have revealed how critical parts of the nerve cell that play a part in the cell's energy metabolism function in the early stages of the disease.

Plaques made up of amyloid-beta-peptide (Aβ) are accumulated in the brains of Alzheimer's patients. The nerve cells of patients with the disease have trouble metabolizing certain substances like glucose and calcium. These disorders are linked to cell death.

The authors explained:

The metabolism of these substances is the job of the cell mitochondria, which serve as the cell's power plant and supply the cell with energy. However, for the mitochondria to do this, they need good contact with another part of the cell called the endoplasmic reticulum (ER). The specialized region of ER that is in contact with mitochondria is called the MAM region.

Previous research on yeast and other types of cells have demonstrated that the contact points between the mitochondria and the ER becomes interrupted by the deactivation of particular proteins in the MAM region. This prevents the delivery of energy to the cell and results in cell death.

Now, the MAM region in nerve cells has been examined for the first time. The experts analyzed the interaction between the mitochondria and the ER in early stage Alzheimer's disease.

At this time in the development of the disease Aβ has not created large, lumpy plaques, however, symptoms are still present, which indicates that Aβ that has not yet formed plaque is harmful to neurons.

The results were somewhat surprising, the investigators said. A rise in the number of contact points between the mitochondria and the ER is seen when nerve cells are exposed to low doses of Aβ. This results in the transfer of more calcium from the ER to the mitochondria.

The consequential over-accumulation of calcium is toxic to the mitochondria and impacts their ability to give energy to the nerve cell.

Maria Ankarcrona, docent and researcher at the Department of Neurobiology, Care Sciences and Society, and the Alzheimer's Disease Research Centre of Karolinska Institutet, said:

"It's urgent that we find out what causes neuronal death if we're to develop molecules that check the disease. In the long run we might be able to produce a drug that can arrest the progress of the disease at a stage when the patient is still able to manage their daily lives. If we can extend that period by a number of years, we'd have made great gains. Today there are no drugs that affect the actual disease process."

The trials were conducted on mice that were bred to develop symptoms of Alzheimer's. Additionally, nerve cells from deceased Alzheimer's patients as well as neurons cultivated in the laboratory were analyzed.

A different study earlier this month indicated that bursts of brain activity may protect against Alzheimer's.

Study sheds new light on Alzheimer (Video Medical And Professional 2020).

Section Issues On Medicine: Disease