Israeli Researchers Achieve Alzheimer’s Breakthrough in Preventing Memory Deterioration in Animal Model
The study introduces a method capable of identifying Alzheimer’s during sleep or anesthesia in the pre-symptomatic stage.
By Pesach Benson, TPS
Offering new prospects for early detection and prevention of Alzheimer’s symptoms, Israeli researchers succeeded in preventing memory deterioration in an animal model.
The Tel Aviv University study unveiled a method capable of detecting Alzheimer’s during sleep or anesthesia in the pre-symptomatic stage, up to 20 years before dementia symptoms emerge. This early detection could revolutionize treatment approaches and significantly improve patient outcomes. The study’s findings were recently published in the peer-reviewed Nature Communications.
The research identified abnormal brain activity in the hippocampus — a key region for memory and learning—during states of anesthesia and sleep. This heightened activity, resulting from neural network destabilization, precedes the onset of Alzheimer’s symptoms. By targeting a small nucleus in the thalamus responsible for regulating sleep states, the researchers managed to suppress this aberrant activity and prevent memory deterioration in the Alzheimer’s animal model.
“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,” said doctoral student Shiri Shoob, 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,” she explained.
Professor Inna Slutsky said that “utilizing Deep Brain Stimulation (DBS) to suppress this nucleus not only inhibited epileptic activity during anesthesia but also prevented memory loss afterward.”
DBS is a surgical procedure used to treat a variety of neurological symptoms, particularly those associated with movement disorders such as Parkinson’s disease, essential tremor, dystonia, and some cases of epilepsy. It involves implanting electrodes within certain areas of the brain and connecting them to a device similar to a pacemaker, which generates electrical impulses. These impulses regulate abnormal brain activity and help alleviate symptoms.
The researchers observed that the DBS treatment administered during the pre-symptomatic phase effectively shielded the animals from memory loss during the symptomatic phase of Alzheimer’s. This suggests a potential therapeutic strategy for intervening early in the disease progression.
“Physiological changes occur in the brain long before the onset of Alzheimer’s symptoms. Our research indicates that the brain possesses mechanisms to protect itself from the disease’s damage, albeit limited,” said Shoob.
The study also shed light on the relationship between Alzheimer’s pathology and postoperative cognitive dysfunction (POCD), a condition prevalent in older individuals undergoing surgery. POCD can manifest as impairments in memory, attention and processing speed. The symptoms are similar to Alzheimer’s, but are temporary, lasting for weeks or months depending on the patient’s age, the anesthesia used, other medications and other factors. The findings could lead to better surgical outcomes, particularly for the elderly.
The researchers now seek to translate their findings into clinical trials involving human subjects.
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