Ozempic’s mention inevitably sparks associations with weight loss. The novel drug, a member of the GLP-1 agonist class, sparked widespread excitement in the medical community when its versatility became apparent: it not only aided individuals in managing their diabetes but also demonstrated potential to lower the risk of cardiovascular disease while inducing rapid weight loss.
Studies suggest that this medication may also provide a protective effect against the development of dementia. Researchers conducted a clinical trial involving more than 200 individuals with mild Alzheimer’s disease, finding that daily injections of a GLP-1 medication for one year significantly slowed the progression of cognitive decline? Researchers found that participants who received the medication showed improved cognitive performance, including better memory recall, linguistic skills, and decision-making abilities, compared to those administered a placebo – an inactive substance designed to mimic the drug’s appearance but not its effect.
The latest findings have been released under the guidance of Dr. Paul Edison at the University of London’s Imperial College.
Launched in 2014, a comprehensive study revealed that liraglutide, a well-established GLP-1 drug approved for both weight management and diabetes treatment in the United States, also possesses neuroprotective properties.
As Alzheimer’s disease progresses, brain cells degenerate at an alarming rate, leading to a progressive decline in cognitive function. During the trial, liraglutide significantly decelerated cognitive decline, resulting in approximately 50% less volume loss in brain regions crucial for memory compared to a placebo control group.
“We’re experiencing a era of unparalleled potential, with novel treatments at various stages of development that may either slow or potentially halt cognitive decline associated with Alzheimer’s disease,” said Dr. Maria C. Dr. Carrillo, Chief Science Officer and Medical Affairs Lead at Alzheimer’s Affiliation, stated… “This analysis suggests a promising future, with additional treatment options potentially available to alter the trajectory of the disease.”
The outcomes were introduced last month online.
Again to Fundamentals
Despite progress in understanding the complexities of Alzheimer’s disease, the quest for effective therapies remains hindered by repeated setbacks. Most therapies constructively exist within the confines of one’s mind. Research suggests that splitting them up could potentially prevent neurons from deteriorating.
Many have experienced limited success. The US Food and Drug Administration (FDA) has approved a medication designed to disintegrate abnormal protein aggregates in individuals displaying initial symptoms of the disease, offering new hope for those diagnosed with this debilitating condition at an early stage. Several weeks after, the European Medicines Agency approved another medication that also targeted these clumps, citing the benefits of slowing cognitive decline as outweighing the risk of significant adverse effects, including brain swelling and haemorrhaging.
Scientists from various disciplines have extensively studied and debated the topic of diabetes elsewhere. Insulin plays a crucial role in maintaining cognitive health, and the presence of Type 2 diabetes poses a significant risk factor for developing Alzheimer’s disease. Can cognitive function be safeguarded through physiological means, specifically targeting metabolic rate, rather than directly addressing protein aggregates in the brain?
Enter GLP-1 medication. When a satisfying meal triggers the release of certain hormones from the stomach, they deceive the brain into believing satiety has been reached. The medication’s effects extend far beyond just the gut—
Researchers found that daily injections of liraglutide for a period of eight weeks significantly prevented memory loss related to Alzheimer’s disease. Their neurons additionally thrived. Synapses, the crucial connectors between brain cells, had surprisingly demonstrated the ability to rapidly form novel neural networks in regions significantly impaired by the disease. Notably, the formation of toxic protein aggregates diminished by a significant 50%, accompanied by a marked reduction in inflammation.
Liraglutide’s efficacy wasn’t solely dependent on its interaction with neurons. In a groundbreaking study using an Alzheimer’s disease mouse model, researchers found that it rapidly modulated the metabolic profile of a distinct subtype of star-shaped glial cells critical for neuronal function. While these cells don’t generate neural networks, they do facilitate energy transmission. While individuals with Alzheimer’s often experience a loss of cognitive function, a remarkable exception was observed when treated with liraglutide, which successfully halted the progression of the disease. The research revealed that the medication enhanced the cells’ ability to support neuronal growth, allowing neurons to thrive and form connections. The mind leveraged its primary energy source, sugar, to fuel the creation of new neurons in a region crucial for memory formation, thereby enabling the initiation of novel cognitive processes.
Despite the sector’s frustration with this fact, mice are, by nature, non-human beings. Promising therapies that excel in mouse studies often fail to translate to humans, earning them the ominous moniker: the “graveyard of desires.”
The Trial
Edison then expanded his inquiry into humans, extrapolating insights gathered from mice to shed light on human physiology and disease mechanisms. Researchers outlined the methodology for a clinical trial designed to assess liraglutide’s efficacy in individuals with mild Alzheimer’s disease. The ELAD study employed a randomized and double-blind design, the industry standard for medical trials. In this double-blind study, both physicians and participants are unaware of whether an individual is receiving liraglutide or a placebo.
Researchers enrolled 204 participants who received either liraglutide or placebo injections daily for a period of 12 consecutive months. Prior to the trial, each participant underwent an MRI examination to create a detailed brain mapping of both structure and function. Various brain imaging techniques captured patterns of mental activity, while a comprehensive set of memory tests meticulously assessed cognitive functioning. The checks were repeatedly conducted at the end, interspersed by security evaluations to detect any unforeseen consequences.
The primary goals of this study were to
One approach was to determine whether liraglutide might boost metabolic activity in brain regions crucial for learning, memory recall, and decision-making processes closely tied to Alzheimer’s disease. As a disease advances, a distinct cognitive capacity steadily diminishes. The final evaluation demonstrated a comprehensive assessment of cognitive functions, encompassing reminiscence, comprehension, linguistic proficiency, and spatial navigation skills.
Research revealed that individuals taking liraglutide experienced a nearly 50% reduction in brain volume loss, with notable improvements seen in regions linked to cognitive function, specifically reasoning and learning abilities. “The reduced pace of cognitive decline implies that liraglutide may have neuroprotective effects, akin to how statins safeguard cardiovascular health.” Edison.
Liraglutide additionally boosted cognition. At various stages of the trial – preceding it, at the halfway mark, and upon completion – patients receiving the medication exhibited a statistically significant 18% slower rate of score deterioration compared to those administered the placebo treatment. Despite these efforts, the drug had no discernible impact on mental metabolism.
While the initial impacts were relatively mild. The commonest was nausea. Severe adverse events, unspecified in number, affected 18 patients but were deemed unrelated to treatment by Edison’s assessment.
Staff presented the outcomes at the convention, although these findings typically hadn’t undergone formal review by experts in the field prior to their public disclosure. Research continues to amass evidence that GLP-1 medications slow the progression of cognitive decline. In June, researchers conducted a simulated trial involving individuals with Type 2 diabetes who received either GLP-1 receptor agonists or two distinct medications, subsequently evaluating cognitive function. According to data gathered from over 88,000 participants across four years, a study reveals that GLP-1 medications outperform two other leading diabetes treatments in preventing dementia onset.
Don’t we wonder how liraglutide safeguards the brain? According to research in mice, various methods may potentially work by reducing inflammation, clearing toxic protein aggregates, and promoting communication between neurons, as Edison explained.
As the notion of sustainable living continues to gain traction. The final stages of investigating semaglutide, the active compound in Ozempic, are currently underway. The proposed research study is expected to span approximately three and a half years, targeting an enrollment of around 1,840 individuals diagnosed with early-stage Alzheimer’s disease. The project is slated for completion by the end of 2026.
“By repurposing medications approved for other indications, we leverage existing knowledge on real-world efficacy, adverse effects, and practical applications, thus streamlining the development process and reducing uncertainty.”
