Memory deterioration prevented in animal model of Alzheimer’s
19 Feb 2024
Suppressing neuronal activity in the part of the brain that regulates sleep can prevent memory deterioration in Alzheimer’s in an animal model, suggests a new study.
Joint work by academics at two universities in Israel identified a method they claim might enable early detection of Alzheimer’s up to two decades before the appearance of any symptoms.
Tel Aviv University doctoral student Shiri Shoob, who led the study, explained that physiological changes slowly and gradually occurred as early as 10-20 years before familiar signs of memory impairment and cognitive decline.
“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.”
Two years ago, TAU researchers from the laboratory of Prof. Inna Slutsky from the Faculty of Medicine and the Segol School of Neuroscience discovered in an animal model there was increased activity in the hippocampus during anesthesia and sleep, resulting from damage to the mechanism that stabilises the neural network pathological brain phenomenon.
Since then, in a study published in Nature Communications, Slutsky’s team, in collaboration with the Safra Center for Neuroscience at the Hebrew University, focused on finding the brain’s protective mechanisms against damage.
They identified that during sleep – particularly following general anesthesia - early symptoms of Alzheimer’s were more easily identified. Prof. Inna Slutsky: “Anesthesia reveals a pathophysiology in the brain activity in the animal model.
They experimented with suppression of neuronal activity in a nucleus of a specific area of the thalamus regulating sleep states, using methods including Deep Brain Stimulation (DBS), often used in the treatment of Parkinson’s and epilepsy.
“In the study, we discovered a connection between the abnormal activity in the hippocampus and a small nucleus called the nucleus reuniens, which connects the thalamus to the hippocampus,” said Slutsky.
“Using DBS to suppress this nucleus inhibited the epileptic activity during anesthesia and prevented memory loss after it. Moreover, DBS treatment during the pre-symptomatic phase prevented memory loss in [the] Alzheimer’s animal model during the symptomatic phase.
Stimulating stimulate the nucleus reuniens at high frequencies, in imitation treatment of Parkinson’s treatment worsened the damage to the hippocampus and the silent seizures said Shoob. But changing to a lower frequency suppressed the seizures and prevented cognitive impairment.
“We showed that the nucleus reuniens had the ability to completely control these seizures. We could increase or decrease the seizures by stimulating it.”
The researchers’ hope is clinical trials in humans could follow with possible benefits for early detection and prevention of the onset of dementia symptoms in Alzheimer’s disease, and in the field of treating postoperative cognitive dysfunction (POCD), cognitive impairments caused by surgery.
PIC: Prof. Inna Slutsky (l, photo - Jonathan Bloom) and Shiri Shoob (r)
