Repositioning GLP-1 Drugs for Neurologic Disease: Evidence, Advances, and Outlook

One of the most searched topics on Google in 2025 was GLP-1s, a class of medications traditionally used to treat type 2 diabetes and in chronic weight management. GLP-1, or glucagon-like peptide-1, is a natural gut hormone that helps regulate blood sugar, appetite, and digestion which these therapies target.

The commercialization and marketization of these medications have become rampant, with drugs like semaglutide (Ozempic/Wegovy) and tirzepatide (Zepbound/Mounjaro) becoming household names akin to Advil and aspirin. Although these therapies have become mainstays in the treatment of metabolic and cardiovascular conditions, there has been significantly increased interest in testing them in neurologic conditions.

The potential neuroprotective effects of GLP-1 was described as early as 2002, predating the FDA approval of the first GLP-1 agent, exenatide (Byetta) Type 2 diabetes in 2005.1 The discovery that GLP-1 receptors are present in the central nervous system (CNS), combined with the ability of GLP-1 receptor agonists (RAs) to cross the blood-brain barrier, positioned them as promising therapeutic candidates for neurological intervention.2

As part of HCPLive’s This Year in Medicine series, we’ll explore how GLP-1 RAs are reshaping thinking across a number of neurological conditions, including Alzheimer disease and other dementias, sleep disorders and obstructive sleep apnea, Parkinson disease, stroke and cardiovascular-brain health, headache and pain conditions, among several other emerging neurologic indications. Together, the sections below provide a comprehensive look at where evidence stands today, where major gaps remain, and how GLP-1 RAs may influence the future of neurologic care.

Alzheimer & Dementia

Dementia remains a major global cause of disability, with prevalence projected to reach roughly 75 million individuals by 2030.3 Diabetes is an important modifiable risk factor, responsible for about 5% of the population-attributable fraction of dementia. In addition, diabetes increases the risk of ischemic stroke, potentially mediating its link to vascular dementia.

There has been a growing body of evidence testing GLP-1 RAs in patients with Alzheimer disease (AD) and related dementias. While promising, the results have been inconsistent to date. Earlier this year, a meta-analysis of 26 randomized trials involving more than 160,000 patients further strengthened the evidence for GLP-1 therapies, showing that, unlike SGLT2 inhibitors, they were associated with a statistically significant reduction in dementia risk and cognitive impairment.4

Despite the success of the large-scale analysis, there were several limitations, including the fact that dementia was captured as an adverse event rather than a prespecified outcome, raising the possibility of misclassification. In addition, the meta-analysis combined heterogenous interventions and variable definitions of dementia outcomes, further pointing to the need for more well-designed, long-term trials.

The most well-designed GLP-1 trial in AD to date was EVOKE (NCT0477396) and EVOKE+ (NCT4777409), 2 massive phase 3 studies that tested semaglutide in patients with early-stage AD who had amyloid-confirmed pathology. The studies, which featured nearly 4000 patients with mild cognitive impairment (MCI) or MCI dementia due to AD, followed individuals for a 2-year period, using change in Clinical Dementia Rating-Sum of Boxes (CDR-SB) as the primary outcome.

The results, recently presented at the 18th Clinical Trials on Alzheimer’s Disease (CTAD) conference, showed that semaglutide did not slow disease progression in these patients despite improvements in certain AD-related biomarkers. A disappointing result, as there was no significant difference between semaglutide and placebo on the primary or secondary end points.5

In the trials, there were some signs of success, as semaglutide-treated patients demonstrated lowered AD-relevant biomarkers in cerebrospinal fluid. These included AD markers like pTau181 (treatment ratio, 0.92), pTau217 (0.91), npT181 (0.90), and npTau205 (0.91), as well as other markers of neuroinflammation (YKL-40; 0.93) and neurodegeneration (total tau: 0.93; neurogranin: 0.92).

Despite the trials not demonstrating efficacy, many feel EVOKE and EVOKE+ represent a large stepping stone in uncovering the true role of GLP-1 RAs in AD care. The Alzheimer’s Association, considered one of the most impactful health organization toward AD care, said that the data, despite it being negative, was “vital to accelerating our understanding of this disease and helps inform the next generation of clinical trials.” The organization added that the data will refine the understanding of this class of drugs, and does not shut the door for future research into other GLPs as means of treatment and prevention.6

Currently, there are 2 ongoing and intriguing studies testing GLP-1 RAs in this field: the phase 2 LIGHT-MCI trial (NCT05313529) and the OxSENSE trial (NCT06363487).

The LIGHT-MCI trial is a prospective, randomized study evaluating whether liraglutide, empagliflozin, or linagliptin–a GLP-1, SGLT2 inhibitor, and DPP-4 inhibitor–can improve cognitive outcomes in patients with type 2 diabetes and MCI inadequately controlled on metformin. Across a cohort of 396 participants, the 48-week core study (with a 28-week extension) uses an unusually comprehensive assessment battery—including metabolic profiling, cognitive testing, olfactory measures, and fMRI—to compare these three drug classes. The trial aims to clarify whether specific glucose-lowering mechanisms can meaningfully alter early cognitive decline, a question gaining momentum as GLP-1–based therapies attract growing interest in neurology.7

OxSENSE, a less intensive trial, tests how a single 0.5-mg dose of semaglutide influences reward sensitivity, cognition, and energy in healthy volunteers, an important topic as GLP-1 agents gain attention for their neurobiological and anti-inflammatory effects. By assessing reward processing, emotional cognition, impulsivity, and activity levels, the study explores whether semaglutide produces neuropsychological changes relevant to depression and whether GLP-1–based therapies could have broader applications beyond metabolic disease.8

Sleep Disorders & OSA

Pharmacologic treatments like GLP-1 RAs, initially developed for blood sugar control, have been increasingly looked at for their ability to reduce body weight and improve obstructive sleep apnea (OSA). The FDA made history last year in approving tirzepatide, marketed as Zepbound, as the first medication for OSA. Overall, this marked a major shift from symptom-based management with continuous airway pressure (CPAP) toward a weight-centered, disease-modifying strategy.9

OSA, which affects an estimated 14% of men and 5% of women, is linked to daytime sleepiness, cognitive impairment, reduced quality of life, and increased risks of cardiovascular disease, diabetes, and stroke. Excess body weight is a significant risk factor for OSA, contributing to airway narrowing and impaired respiratory mechanics. In addition, OSA and weight gain have a bidirectional relationship, as OSA can also promote weight gain by disrupting sleep.

A meta-analysis published earlier this year in the journal of Sleep Medicine looked at 3 trials evaluating GLP-1 RAs for OSA in adults with a body mass index of at least 30 kg/m2, which is considered the threshold for obesity. Led by Kaeshaelya Thiruchelvam, PhD, of the Univeristy of Newcastle, this class of drugs was found to be quite effective, leading to a weight mean difference of –16.6 apnea-hypopnea index (AHI) events per hour. One notable downside: GLP-1 RAs were associated with a higher frequency of safety events, with an odds ratio of 1.62 (95% CI, 1.16-2.24) compared with placebo.10

Upon its approval, the FDA noted tirzepatide should be used in combination with a reduced-calorie diet and exercise. Currently, more research is needed to inform the use of GLP-1 agonists as a potential standalone therapy for OSA.

Parkinson Disease

Over the years, GLP-1 RAs have been repurposed in movement disorders based on their ability to engage mechanisms beyond glucose control. For Parkinson disease (PD), the current therapies have problems with short half-life and fluctuant plasma levels of levodopa, the precursor of dopamine.

In August, one of the largest systematic reviews assessing GLPs in PD, published by Mohamed Mohsen Helal, MD, et al, further showcased the potential for these treatments. Of the 1426 records reviewed, 46 studies were identified as potentially relevant, and 5 were included in the final analysis. Published in Diabetology & Metabolic Syndrome, the use of this class of therapies led to significantly improved motor function, as reflected by MDS-Unified Parkinson’s Disease Rating Scale- Part III scores in the ON state (mean difference, –2.88; P = .001; I2 = 30%).11

“When it comes to neurodegenerative diseases, no single component can address their pathophysiology, at least at this time point,” Helal told NeurologyLive. “This is a fact that we should all be aware of. Neurodegenerative diseases are now thought of as having multiple theories and intervening pathologies, from genetics to environmental factors and lifestyles—not a single causality. We should target and exert more effort, money, and research into neurodegenerative and movement disorder prevention rather than awaiting the disease to develop.”

Helal went on to say that the question of “which population is most likely to benefit from a GLP-1” cannot be answered now with the level of evidence currently available. He went on to say that the clinical community should focus more on which agent might be more beneficial in this population.

“As of December 2025, we have 6 published trials of GLP-1 therapies in PD with 4 members of the GLP-1 family tried,” he noted. “The results are mixed: Exenatide failed to meet a significant efficacy profile in 2 trials and trials for liraglutide and NLY01 were inconclusive, whereas lixisenatide, studied in the LIXIPARK trial by Meissner and colleagues, showed superiority to placebo and significant potential.”

Lixisenatide, a once-daily treatment given as a subcutaneous injection, was tested in a phase 2 placebo-controlled trial of patients with PD who had been living with the diagnosis for less than 3 years. The trial, published in the New England Journal of Medicine, showed that treatment with the medication resulted in less progression of motor disability than placebo at 12 months, although it was associated with gastrointestinal adverse effects. At 14 months, after a 2-month washout period, the mean MDS-UPDRS motor scores in the off-medication state were 17.7 (95% CI, 15.7 to 19.7) with lixisenatide and 20.6 (95% CI, 18.5 to 22.8) with placebo.12

Another placebo-controlled trial that drew some clinical attention focused on the use of exenatide, a GLP-1 used for type 2 diabetes, and its brain metabolic effects in PD. Presented at the 2025 MDS Congress, held October 5-9 in Hawaii, a double-blind, placebo-controlled trial (n = 59) showed that use of this medication led to significant effects on PD-related motor expression (P = .001) over a 9-month period, although more research is needed.13

Stroke & Cardiovascular Health

GLP-1 RAs look promising for stroke and brain health from 2 main angles: vascular risk modification and possible direct neuroprotection. Beyond their glycemic effects, GLP-1 RAs reduce systemic inflammation, improve endothelial function, lower blood pressure, and favorably after lipid profiles—mechanisms supported across multiple cardiovascular outcome trials.

There were several notable updates and trials involving GLP-1 RAs in the stroke field in 2025, none bigger than semaglutide's EU approval as the first stroke management therapy. The EMA’s decision, which came in September, stamped semaglutide with documented benefits in reducing cardiovascular death, heart attack, and stroke.14

Data from the phase 3 SOUL trial (NCT03914326) was the leading driver behind this decision. In this study of nearly 10,000 patients, treatment with semaglutide led to a 14% reduction in cardiovascular death, heart attack, and stroke vs placebo when added to the standard of care in adults with type 2 diabetes at high cardiovascular risk.15 Of note, regulatory action in the US is expected by the end of this year on whether semaglutide will gain an expanded label to cover cardiovascular risk reduction.

Semaglutide was also featured in the first head-to-head trial testing GLP-1 RAs in improving cardiovascular health and stroke risk. Presented at the European Association for the Study of Diabetes (EASD) 2025 Annual Meeting, the target trial emulated study included 58,336 matched patients or older with established atherosclerotic cardiovascular disease (ASCVD) to either once-weekly semaglutide or dulaglutide, another competitor GLP-1.

All told, treatment with semaglutide led to a 26% lower risk of death vs dulaglutide, and a 23% reduced risk of heart attack, stroke, and death.16 These data, some of the first comparative findings announced, reinforced the established clinical evidence of semaglutide, and further added evidence to a knowledge gap about how specific therapies perform.

In the weeks following the EASD data, a new real-world study dubbed STEER further added to the individual impact of GLP-1 RAs in reducing heart attack and stroke. In this large retrospective analysis of adults with overweight or obesity and established cardiovascular disease—but no diabetes—semaglutide 2.4 mg (n = 10,625) demonstrated a 57% greater reduction in major cardiovascular adverse events, cardiovascular-related death, or all-cause death compared with tirzepatide (n = 10,625).17

Over the course of the year, there has also been a significant uptick in the research related to GLP-1 RAs and idiopathic intracranial hypertension (IHH), a condition that impacts around 1 per 100,000 people. IHH, characterized by elevated intracranial pressure in the absence of a detectable cause, leads to symptoms like headache, visual disturbances, and pulsatile tinnitus.

A study of more than 44,000 patients with IHH from the TriNetX US Collaborative Network revealed that those on GLP-1 RAs were less likely to require any medication compared with the control group (29.7% vs 56.4%; P <.001) and demonstrated significantly lower mortality (≤2.0% vs 5.0%; P = .003). More notably, GLP-1 users had lower prevalence of IIH symptoms such as headache (12.3% vs 27.4%; P <.001), visual disturbances/blindness (7.0% vs 11.7%; P = .007), and papilledema (2.2% vs 11.5%; P <.001).18

Through these data, GLP-1 RAs show promise as a disease-modifying therapy for IIH, with potential benefits beyond weight loss. The consistency of these findings was proven across multiple studies and data sources and further pooled together in a systematic review published in The Journal of Headache and Pain in October. In their conclusion, the study authors, including Julien Ognard, PhD, an associate professor at University of Western Brittany, noted the significance of the data also supports a well-powered phase 3 randomized controlled trial to validate what was seen and define optimal treatment strategies.19

Headache & Pain Disorders

GLP-1 is widely expressed in the central and peripheral nervous system, where it influences neuroinflammation, neuronal excitability, and nociceptive processing. These effects extend beyond its metabolic role and highlight GLP-1 as an important neuromodulator involved in pain pathways.

Because GLP-1 signaling can reduce inflammatory activity and central sensitization, there is potential for GLP-1 RAs to be explored as treatments for headache and other pain disorders. Early evidence suggests these medications may modulate pain circuits and neuroimmune responses that contribute to chronic migraine; however, more data are needed.

“At present, there is no mechanistic rationale supporting the use of GLP-1 receptor agonists as a treatment for headaches or migraine. A few emerging findings suggest that this pathway may deserve deeper investigation, potentially through a dedicated phase 2 clinical trial,” neurologist Lanfranco Pellesi, MD, told NeurologyLive.

Pellesi, an assistant professor of clinical pharmacology, pharmacy, and environmental medicine at the University of Southern Denmark, went on to add, “The most compelling evidence comes from IIH, where preliminary studies indicate that GLP-1 receptor agonists may provide benefit, likely because GLP-1 signaling helps regulate intracranial pressure via effects on the choroid plexus. In migraine, the data are more limited. We still do not understand whether GLP-1 activity can influence the pain pathways involved in migraine pathophysiology. Overall, while intriguing signals exist, the field currently lacks the mechanistic and clinical evidence needed to justify therapeutic use.”

Pellesi was among the study authors for a 2024 systematic review looking at trials of GLP-1 RAs in headache and pain disorders. A total of 42 animal and human studies were included in the final review, spanning 4 categories: inflammatory pain and osteoarthritis, headaches, neuropathic pain and diabetic neuropathy, and visceral pain and irritable bowel syndrome.20

Within the headache section, 1 notable trial, a randomized, placebo-controlled study of women with active IIH, revealed that exenatide reduced intracranial pressure at 2.5 hours, 24 hours, and 12 weeks, and produced a meaningful reduction in monthly headache days (−7.7 vs. −1.5). Notably, this improvement occurred without significant BMI change, suggesting a direct physiologic effect on CSF dynamics rather than weight loss.

To date, obesity is a major modifiable risk factor for chronic migraine, contributing to central sensitization and exacerbating the frequency and severity of attacks. Weight loss can alter headache patterns in some patients. During digestion, intestinal peptides such as GLP-1 and amylin are released and slow gastric emptying. At the same time, glucagon from the pancreas and gastric leptin help regulate appetite by signaling satiety to the brain, which reduces food intake.

A prospective, open-label, pilot study published earlier this year explored the effectiveness and tolerability of liraglutide as an add-on treatment for those with obesity and high-frequency chronic migraine. While the study excluded cases suspected of IIH, 31 patients with unresponsive migraine were included, most of which were women (n = 26; 83.8%).

Published in Headache, the study found that use of liraglutide as an add-on had a significant effect in headache days, the primary end point, with patients showing a mean decrease from 19.8 to 10.7 days post-treatment. Conversely, BMI decreased slightly from a mean of 34.0 (SD, 2.3) to 33.9 (SD, 2.3) kg/m2, although this change was not significant (mean difference, 0.1 kg/m2; 95% CI −0.004 to 0.153 kg/m2; P = .060; Cohen d = 0.34). More notably, a simple linear regression analysis revealed that BMI reduction did not significantly predict did not significantly predict headache frequency reduction (β = −1.448; 95% CI −19.390 to 16.495; P = .870; R2 = 0.001), indicating no meaningful relationship between the 2 variables.21

“Two major questions remain unanswered: Do GLP-1 receptor agonists work for migraine, and why would they work? As of today, we lack a randomized, placebo-controlled trial showing that GLP-1 receptor agonist therapy can prevent migraine attacks more effectively than placebo,” Pellesi added.

“My own thinking is that if these agents are effective, they are more likely to act as preventive rather than acute treatments, but this remains speculative. The mechanistic gap is equally significant. We do not yet know which GLP-1 receptors might mediate analgesic effects in migraine, and they are unlikely to be the same receptors responsible for metabolic benefits in diabetes and obesity. Although GLP-1 receptors are expressed along nociceptive pathways, it is unclear whether neuronal or glial populations are involved, and we have no data on their role within the trigeminal system, the key circuitry in migraine,” Pellesi concluded. “Much fundamental work is still needed.”

GLP-1 RAs On the Horizon

There are several other areas of neurology where GLP-1 RAs are starting to make headway but haven’t reached mid or late-stage clinical trial settings. Some of these include traumatic brain injury/neurotrauma, chronic pain and neuropathy, mood disorders, and neuroimmune or demyelinating diseases, like multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD).

A large-scale, retrospective study presented earlier this year at the American Academy of Neurology (AAN) meeting compared 7046 adults with MS receiving oral and injectable GLP-1 agonists to matched patients not receiving treatment for a 5-year period. Led by Elizabeth Morrison-Banks, MD, a board-certified neurologist at Riverside Community Hospital, those not treated with GLPs had significantly more MS disease progression, including higher risk of brainstem dysfunction (4.36% risk difference, P <.0001), cerebellar dysfunction (4.54% risk difference, P <.0001), and bowel/bladder dysfunction (4.98% risk difference, P <.0001).22

In other neuroimmune conditions, a first-of-its-kind study identified that GLP-1 and GLP-1 receptor contributes to brain inflammation and nerve overactivity, leading to area postrema syndrome (APS), a hallmark feature for patients with NMOSD. When comparing healthy controls and non–APS-attacked NMOSD, APS-attacked patients with the disease demonstrated significantly elevated GLP-1/GLP-1R levels in plasma and cerebrospinal fluid (CSF) and gradually decreased after immunotherapy.23

Study authors, including Lingfei Yang, PhD, a physician at the First Affiliated Hospital of Zhengzhou University, in China, noted that the findings don’t necessarily mean that GLP-1 drugs are automatically harmful or cause inflammation on their own. Instead, the findings suggest that these therapies may trigger strong reactions in patients who already have inflammation in the brain, such as those with NMOSD, although more research is needed.

Exenatide was also tested in a proof-of-concept trial in patients with multiple system atrophy (MSA), a movement disorder with no approved treatments. The single-center study, published earlier this year, included 50 patients, showed that patients on the GLP-1 had slowed disease progression, as exemplified through the Unified MSA Rating Scale (6.1 points; 95% CI, 3.0-9.3), compared with the control group (13.3 points; 95% CI, 9.2-17.3; P = .0003). Notably, there were no statistically significant differences at either 48 or 96 weeks on secondary outcomes, and imaging findings were also similar between the 2 groups.24

The study authors noted that the data do not support the use of exenatide in patients with MSA, as there were no clear advantages on several measures, including falls, bulbar impairment, mortality, gait activity, or MRI regional volumes.

As research accelerates, GLP-1–based therapies are poised to remain a major focus in neurology, with expanding evidence suggesting they may influence neuroinflammation cerebrovascular health, protein aggregation, and metabolic contributors to neurologic disease. Although many questions persist—including optimal dosing, long-term safety in neurologic populations, and the degree to which metabolic vs direct neurobiological effects drive outcomes—the momentum behind GLP-1 research signals a transformative period ahead. For neurologists, the coming years may redefine how metabolic pathways intersect with brain health and open new therapeutic avenues across multiple domains of neurologic care.

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