Researchers prevent memory deterioration in Alzheimer’s model
Research team at Tel Aviv University may have found way to predicting the disease in dormant state, before onset of cognitive decline.
Researchers at Tel Aviv University, in collaboration with the Safra Center for Neuroscience at the Hebrew University, have found ways to prevent abnormal brain activity and subsequent cognitive impairment in in an animal model of Alzheimer’s disease. One of the methods is Deep Brain Stimulation (DBS), which is a well-known method used in the treatment of Parkinson’s and epilepsy.

In addition, the researchers discovered a method with the potential for early detection of Alzheimer’s during sleep or anesthesia in the pre-symptomatic stage, between 10-20 years before the onset of dementia symptoms [1].

Longevity.Technology: In 2022, a team of researchers from the laboratory of Professor Inna Slutsky from the Faculty of Medicine and the Segol School of Neuroscience at TAU uncovered a pathological brain phenomenon in in an animal model that precedes the first appearance of Alzheimer’s disease symptoms by many years. This is an increased activity in the hippocampus during the states of anesthesia and sleep, which results from damage to the mechanism that stabilizes the neural network [2].

Building on that work, Slutsky’s laboratory team, working with the Safra Center for Neuroscience, have found that suppression of neuronal activity in a small nucleus in a specific area of the thalamus (which regulates sleep states) caused a decrease in pathological activity in the hippocampus and prevented the deterioration of the memory in Alzheimer’s in an animal model.

The researchers hope that their research, which has been published in Nature Communications, will speed up the start of clinical trials in humans, lead to progress in the fields of early detection and prevention of the onset of dementia symptoms in Alzheimer’s disease, and in the field of treating cognitive impairments caused by surgery (POCD – Postoperative Cognitive Dysfunction).

“As early as 10-20 years before the appearance of the familiar symptoms of memory impairment and cognitive decline, physiological changes slowly and gradually occur within the patients’ brains,” explains Shiri Shoob, a doctoral student who led the study.

“There is an accumulation of amyloid-beta deposits and abnormal accumulations of tau protein, a decrease in the volume of the hippocampus, and more. Moreover, about 30% of the people who were found to have a pathology typical of Alzheimer’s disease at postmortem did not develop the typical symptoms of the disease during their lifetime. It seems, then, that the brain has an, admittedly limited, ability to protect itself from the damage of the disease.”

The research focused on finding those protective mechanisms which the brain has to combat damage from the disease. The researchers found that during sleep – and especially during sleep as a result of general anesthesia – the early symptoms of Alzheimer’s disease, which appear many years before the symptoms of dementia, could be more easily identified. Professor Slutsky said: “Anesthesia reveals a pathophysiology in the brain activity in the animal model. We think that there are mechanisms that compensate for that same pathology while awake and thus prolong the pre-symptomatic period of the disease.”

The researchers identified hyperactivity in the hippocampus – so-called ‘silent seizures’ that resemble epileptic seizures in terms of brain activity, but do not appear externally – in in an animal model of Alzheimer’s disease. This finding is in contrast to the usual reduced activity during sleep and anesthesia in the healthy hippocampus. To examine potential treatment and prevention measures, the researchers tried a variety of methods, but mainly focused on deep brain stimulation (DBS) using electrical signals to the nucleus reuniens – a small nucleus in the brain that connects the affected hippocampus and the thalamus, which is responsible for sleep regulation.

Researchers prevent memory deterioration in Alzheimer’s model