Israeli researchers have achieved a significant breakthrough by preventing memory deterioration in an animal model, thereby presenting promising avenues for early detection and prevention of Alzheimer’s disease.
The study, conducted at Tel Aviv University and recently published in Nature Communications, introduces a groundbreaking approach capable of identifying Alzheimer’s in the pre-symptomatic stage, potentially up to 20 years before the onset of dementia symptoms. This pioneering method holds the promise of revolutionizing treatment strategies and significantly improving patient outcomes.
Researchers discovered abnormal brain activity in the hippocampus, a critical area 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, researchers effectively suppressed this abnormal activity and prevented memory deterioration in the Alzheimer’s animal model.
Leading the study, doctoral student Shiri Shoob said that physiological changes begin occurring in the brain 10-20 years before the emergence of familiar symptoms. These changes include the accumulation of amyloid-beta deposits, abnormal accumulations of tau protein, a decrease in hippocampal volume, and more.
Interestingly, approximately 30% of individuals with postmortem evidence of Alzheimer’s pathology did not exhibit typical symptoms during their lifetime, suggesting the brain’s limited ability to protect itself.
Professor Inna Slutsky highlighted the potential of Deep Brain Stimulation (DBS) not only to suppress epileptic activity during anesthesia but also to prevent subsequent memory loss. DBS, a surgical procedure for neurological symptoms, involves implanting electrodes in the brain connected to a device generating electrical impulses. These impulses regulate abnormal brain activity, providing relief from symptoms.
Administering DBS during the pre-symptomatic phase effectively shielded animals from memory loss during the symptomatic phase of Alzheimer’s, indicating a potential therapeutic strategy for early intervention in the disease’s progression. Shoob said that physiological changes in the brain precede Alzheimer’s symptoms, suggesting the brain has mechanisms to protect itself, albeit limited.
The study also shed light on the connection between Alzheimer’s pathology and postoperative cognitive dysfunction (POCD), a temporary condition in older individuals undergoing surgery. POCD shares symptoms with Alzheimer’s, such as impairments in memory, attention, and processing speed. These findings hold promise for improving surgical outcomes, particularly for the elderly.
The researchers aim to translate their findings into clinical trials involving human subjects, marking a promising step toward advancing Alzheimer’s research and treatment.