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GLP-1 Agonists & Neurodegeneration Research

Few topics in neuroscience have generated as much excitement -- and as much confusion -- as the idea that diabetes drugs might protect the brain from degenerative diseases.

Few topics in neuroscience have generated as much excitement -- and as much confusion -- as the idea that diabetes drugs might protect the brain from degenerative diseases. GLP-1 receptor agonists like semaglutide and liraglutide have dominated headlines with reports linking their use to lower rates of Alzheimer's and Parkinson's disease. The preclinical data looked remarkable. The epidemiological signals were striking. Then came the clinical trial results, and the picture got complicated.

This article walks through the full evidence: how GLP-1 receptors work in the brain, what animal studies have shown, the results from major clinical trials (including the closely watched EVOKE trials), what real-world data from diabetes registries tells us, the proposed biological mechanisms, and what all of this means for patients and researchers moving forward.

The short version: the story is far from over, and the answer may depend on a distinction between treatment and prevention.

Table of Contents

GLP-1 Receptors in the Brain {#glp-1-receptors-in-the-brain}

The neuroprotection story begins with a basic biological fact: GLP-1 receptors aren't just in the pancreas and gut. They're distributed throughout the central nervous system, with particularly high expression in brain regions that matter most for cognitive function.

GLP-1 receptors have been identified in the hippocampus (the brain's memory center), the cortex (responsible for higher-order thinking), the hypothalamus, the amygdala, the cerebellum, and the brainstem. The brain also produces its own GLP-1 in the nucleus tractus solitarius and certain hypothalamic nuclei, meaning it has a local signaling system in addition to receiving GLP-1 from the periphery.

The question of whether medications can reach these brain receptors is important. Research has shown that both labeled GLP-1 and exendin-4 (the molecule behind exenatide) were detected in the cerebellum, cortex, hippocampus, hypothalamus, and brainstem within just 10 minutes of peripheral infusion. When researchers blocked GLP-1 receptors, this brain entry was markedly reduced, confirming a receptor-mediated transport mechanism across the blood-brain barrier (Frontiers in Physiology, 2020).

This distribution pattern positioned GLP-1 agonists as plausible candidates for neurological intervention long before the first clinical trials began. The neuroprotective potential of GLP-1 was actually described as early as 2002 -- three years before the FDA approved exenatide for type 2 diabetes.

The Brain Energy Deficit: Why Diabetes and Dementia Are Connected {#brain-energy-deficit}

To understand why diabetes drugs might help with brain diseases, you need to understand what Alzheimer's and Parkinson's have in common at a cellular level.

Both are chronic neurodegenerative disorders characterized by something often overlooked: the brain stops using glucose efficiently. In the brains of Alzheimer's and Parkinson's patients, insulin signaling and insulin-like growth factor 1 (IGF-1) signaling become impaired early in the disease process. This "brain insulin resistance" leads to a cascade of problems:

  1. Neurons can't take up glucose properly, starving them of their primary fuel
  2. Mitochondrial function deteriorates, reducing energy production further
  3. Despite the brain attempting to compensate by using ketones and amino acids, the energy deficit grows
  4. Without enough energy, neurons can't maintain synaptic connections, repair cellular damage, or clear misfolded proteins
  5. Toxic proteins accumulate (amyloid-beta in Alzheimer's, alpha-synuclein in Parkinson's), and neurons die

This energy deficit framework explains one of the strongest epidemiological links in medicine: type 2 diabetes roughly doubles the risk of developing Alzheimer's disease. Both conditions share impaired insulin signaling, chronic inflammation, and mitochondrial dysfunction -- and GLP-1 receptor agonists address all three.

As researchers from CNS Drugs, 2025 put it: incretin hormones like GLP-1 can normalize energy use and reduce inflammation in the brain, making them logical candidates for repurposing against neurodegenerative conditions.

Preclinical Evidence: What Animal Studies Show {#preclinical-evidence}

The preclinical case for GLP-1 agonists in neurodegeneration is extensive. Dozens of studies in animal models of both Alzheimer's and Parkinson's disease have reported positive results, though the picture isn't perfectly clean.

Alzheimer's Disease Models

In APP/PS1 transgenic mice (a standard Alzheimer's model), liraglutide reduced amyloid-beta plaque counts by 40-50% in the cortex and hippocampus, and cut the number of activated inflammatory microglia by 50%. It also preserved the insulin receptor signaling pathways that deteriorate in Alzheimer's by activating the PKA signaling pathway (Frontiers in Neuroscience, 2022).

Semaglutide has shown improved cognitive function and reduced neuroinflammation in APP/PS1 mice, working through AMPK activation and inhibition of the TLR4/NF-kB inflammatory pathway. In another study, semaglutide improved Alzheimer's pathology in both mouse models and human brain organoids.

GLP-1 analogs have also been shown to protect hippocampal synapses from the toxic effects of amyloid-beta. When researchers injected amyloid-beta directly into the brain, GLP-1 agonists preserved long-term potentiation (LTP) -- the cellular process underlying memory formation -- by preventing calcium overload and improving mitochondrial function.

Parkinson's Disease Models

In 6-OHDA models of Parkinson's disease (which selectively destroy dopamine-producing neurons), semaglutide protected neurons by boosting autophagy (cellular cleanup) and reducing oxidative stress. Other GLP-1 agonists have shown similar dopaminergic neuron protection across multiple Parkinson's models.

Conflicting Results

Not all preclinical data points in the same direction. One study found that semaglutide and tirzepatide did not alter disease-related pathology, behavior, or cognitive function in 5XFAD and APP/PS1 mice. This inconsistency highlights that animal models don't always predict human outcomes and that the therapeutic window, dosing, and timing of intervention may all matter.

Clinical Trial Results {#clinical-trial-results}

The gap between promising animal data and clinical reality has proven wide. The major clinical trials testing GLP-1 agonists against established neurodegenerative disease have produced mixed-to-disappointing results on their primary endpoints, though with some intriguing secondary signals.

The ELAD Trial: Liraglutide in Alzheimer's {#elad-trial}

The Trial: Led by Professor Paul Edison at Imperial College London, ELAD was a randomized, double-blind, placebo-controlled phase 2b trial. 204 patients with mild Alzheimer's disease at 24 UK clinics received either liraglutide (up to 1.8 mg daily by subcutaneous injection) or placebo for 12 months. Patients underwent MRI brain scans, glucose metabolism PET scans, and detailed cognitive testing before and after the study.

Primary Endpoint: Change in cerebral glucose metabolic rate in cortical brain regions. Result: Not met. No significant differences in brain glucose metabolism between the treatment groups.

Secondary Findings: This is where things got interesting.

  • Liraglutide appeared to reduce brain shrinkage by nearly 50% compared to placebo across several brain regions, including frontal, temporal, parietal, and total gray matter, as measured by MRI (Nature Medicine, 2025)
  • As Professor Edison described it: "The slower loss of brain volume suggests liraglutide protects the brain, much like statins protect the heart"
  • Serious side effects were actually less common in the liraglutide group (7%) than the placebo group (18%)
  • The most common side effects were gastrointestinal (nausea, diarrhea, vomiting), affecting about 25% of participants, usually mild and temporary

The ELAD trial didn't prove that liraglutide treats Alzheimer's, but the brain volume preservation signal was striking enough to help justify the much larger semaglutide trials that followed. The Alzheimer's Drug Discovery Foundation invested nearly $1 million in ELAD beginning in 2011, and the results catalyzed subsequent funding from Novo Nordisk for the phase 3 EVOKE program.

EVOKE and EVOKE+: Semaglutide in Alzheimer's {#evoke-trials}

The Trials: EVOKE and EVOKE+ were the most anticipated GLP-1 trials in neurodegeneration -- two large-scale, randomized, double-blind, placebo-controlled phase 3 studies evaluating oral semaglutide (up to 14 mg daily) versus placebo in early-stage Alzheimer's disease. Together they enrolled more than 3,600 participants aged 55-85 years with mild cognitive impairment or mild dementia due to Alzheimer's, confirmed by amyloid biomarker abnormalities. EVOKE+ also allowed patients with concomitant small-vessel cerebrovascular disease (Alzheimer's Research & Therapy, 2024).

The treatment period was 156 weeks (3 years), with a primary endpoint measuring functional decline on the Clinical Dementia Rating-Sum of Boxes (CDR-SB) scale at 104 weeks.

Primary Result: The trials failed. Oral semaglutide did not slow cognitive or functional decline compared to placebo. For every primary and secondary cognitive and functional outcome, the curves for the semaglutide and placebo groups were virtually indistinguishable over the three-year study period (NeurologyLive, 2025).

After seeing no effect on the primary endpoint, Novo Nordisk canceled the planned one-year extension of both trials.

Biomarker Signals: Despite the clinical failure, semaglutide-treated patients showed improvements in several Alzheimer's-related biomarkers measured in cerebrospinal fluid:

  • Lowered pTau181 and pTau217 (markers of tau pathology)
  • Reduced YKL-40 (a neuroinflammation marker)
  • Decreased total tau and neurogranin (markers of neurodegeneration)

These biomarker shifts were only seen in CSF, not in blood, and were "nominally significant" -- meaning they showed trends but weren't strong enough to overcome multiple comparison corrections.

Reaction: The Alzheimer's Drug Discovery Foundation called the results a "fundamental shift in how we approach the development of new Alzheimer's treatments, expanding beyond amyloid to target the complete pathobiology of the disease." Others were more blunt: the drug didn't work for treating established Alzheimer's, regardless of what the biomarkers suggested (Science, 2025).

Parkinson's Disease Trials {#parkinsons-trials}

LIXIPARK (Lixisenatide): Published in the New England Journal of Medicine, 2024, this phase 2 trial randomized 156 patients with early Parkinson's disease to daily lixisenatide or placebo for 12 months, followed by a 2-month washout.

Results: At 12 months, motor disability scores on the MDS-UPDRS Part III (measured while on medication) changed by -0.04 points with lixisenatide (essentially stable) versus +3.04 points with placebo (worsening), a statistically significant difference (p=0.007). After the 2-month washout, the difference persisted, which some researchers interpret as evidence of disease modification rather than just symptomatic relief.

However, secondary endpoints including patient-reported symptoms did not confirm the slowing of progression. Nausea occurred in 46% of participants taking lixisenatide, raising concerns about unblinding that could bias motor assessments. The investigators explicitly cautioned against off-label use of GLP-1 agonists for Parkinson's until larger trials confirm the findings.

Exenatide Phase 3: Early in 2025, results from a large phase 3 trial of exenatide in Parkinson's disease showed no slowing of disease progression, despite encouraging results from an earlier phase 2 study. This was another example of promising early-phase data not translating into later-stage success.

Real-World Evidence From Diabetes Registries {#real-world-evidence}

While the clinical trials for treatment have been discouraging, a different type of evidence has been building steadily: people who take GLP-1 agonists for diabetes appear to develop dementia at lower rates.

Key Epidemiological Studies

Danish Registry + Pooled RCT Data: A landmark study combined data from three randomized cardiovascular outcome trials (15,820 patients) with nationwide Danish registry data (120,054 patients). In the RCT pool, patients randomized to GLP-1 agonists had a 53% lower rate of dementia compared to placebo (HR 0.47; 95% CI 0.25-0.86). In the registry cohort, each additional year of GLP-1 agonist exposure was associated with an 11% reduction in dementia (HR 0.89; 95% CI 0.86-0.93) (PubMed, 2022).

Swedish National Registers: A study emulating a three-arm trial using Swedish registry data (88,381 participants, 4,607 dementia cases) found GLP-1 agonists were associated with a 30% lower dementia risk compared to sulfonylureas and a 23% lower risk compared to DPP-4 inhibitors. The incidence rate for GLP-1 agonist users was 6.7 per 1,000 person-years, compared to 11.8 for DPP-4 inhibitors and 13.7 for sulfonylureas (eClinicalMedicine, 2024).

TriNetX Global Network: A retrospective cohort study of 165,378 individuals using propensity-score matching found GLP-1 agonist use was associated with a 42% reduction in overall dementia risk, along with substantial reductions in Alzheimer's disease and vascular dementia specifically (PMC, 2025).

Taiwanese Population Study: Among 109,778 individuals, GLP-1 agonist use showed a reduced dementia risk (aHR 0.90; 95% CI 0.83-0.97) (PMC, 2025).

Meta-Analysis: A meta-analysis by Seminer et al. spanning 26 studies reported a significant reduction in dementia and cognitive impairment among GLP-1 agonist users (OR 0.55; 95% CI 0.35-0.86).

Why DPP-4 Inhibitors Make a Good Comparison

One finding strengthens the case for direct brain effects. DPP-4 inhibitors also raise GLP-1 levels in the blood, but they do so indirectly and have limited blood-brain barrier penetration. The consistent finding that GLP-1 agonists outperform DPP-4 inhibitors in reducing dementia risk suggests the neuroprotective effect depends on direct activation of GLP-1 receptors within the brain, not just systemic metabolic improvement (British Journal of Clinical Pharmacology, 2025).

Important Caveats

These are observational studies, not randomized trials. They cannot prove causation. Possible confounders include:

  • Healthier patients may be more likely to receive GLP-1 agonists
  • GLP-1 agonist users may have better overall healthcare engagement
  • Cardiovascular risk reduction (preventing strokes, improving blood flow) could independently reduce dementia risk
  • Differences in diabetes severity, socioeconomic status, and other medications may not be fully adjusted for

Still, the consistency of findings across different countries, healthcare systems, comparator drugs, and statistical methods makes the signal hard to dismiss entirely.

Proposed Mechanisms of Neuroprotection {#proposed-mechanisms}

If GLP-1 agonists do protect the brain, how would they do it? Researchers have identified several overlapping pathways, which connect directly to the known pathology of Alzheimer's and Parkinson's disease.

Reducing Neuroinflammation

Chronic neuroinflammation is increasingly recognized not as a side effect of neurodegeneration, but as a primary driver. Overactivated microglia (the brain's immune cells) release toxic inflammatory cytokines that damage neurons and synapses.

GLP-1 receptor activation suppresses this inflammatory cascade through several routes:

  • Inhibiting the NLRP3 inflammasome pathway
  • Promoting anti-inflammatory M2 microglial polarization
  • Reducing TNF-alpha, IL-6, and IL-1-beta in the brain
  • Suppressing NF-kB signaling, a master inflammatory regulator

The EVOKE trials confirmed some of this in humans: semaglutide reduced CSF levels of YKL-40, a marker of neuroinflammation, even though it didn't improve clinical symptoms.

Restoring Brain Insulin Signaling

In Alzheimer's patients, brain insulin receptor expression and signaling are impaired. GLP-1 receptor agonists can restore insulin signaling in the brain through their shared downstream pathways -- both GLP-1 receptor and insulin receptor signaling converge on the neuroprotective PI3K/Akt pathway.

In animal models, liraglutide prevented the loss of brain insulin receptors caused by amyloid-beta oligomers and normalized insulin signaling even in the streptozotocin rat model of Alzheimer's. This extends to non-human primates as well, suggesting the mechanism translates across species.

Reducing Amyloid and Tau Pathology

  • GLP-1 receptor activation reduces BACE1 activity (the enzyme that produces amyloid-beta) through AMPK activation and GSK-3-beta inhibition
  • Liraglutide reduced total amyloid plaque burden by 40-50% in mouse models
  • In the EVOKE trials, semaglutide lowered CSF pTau181 and pTau217 -- direct markers of tau pathology -- suggesting it can influence the protein aggregation that defines Alzheimer's at a molecular level

Protecting Synapses and Promoting Neurogenesis

GLP-1 receptor signaling in the hippocampus supports synaptic transmission, promotes neurogenesis (the birth of new neurons), and protects existing synapses from amyloid-beta toxicity. GLP-1 analogs improve long-term potentiation -- the cellular process underlying learning and memory -- by preventing calcium overload and supporting mitochondrial function.

Improving Mitochondrial Function

GLP-1 receptor signaling activates AMPK, which in turn stimulates PGC-1-alpha-dependent mitochondrial biogenesis. This is directly relevant because mitochondrial dysfunction and energy failure are early features of both Alzheimer's and Parkinson's disease. By supporting cellular energy production, GLP-1 agonists may address one of the fundamental upstream problems in neurodegeneration.

Vascular Protection

Given the strong evidence for cardiovascular benefits of GLP-1 agonists, it's worth noting that vascular health and brain health are tightly linked. Improved endothelial function, reduced atherosclerosis, and stroke prevention all contribute to better brain perfusion and lower risk of vascular dementia. Some of the "neuroprotective" effect seen in registry studies may partly reflect cardiovascular protection.

Next-Generation Approaches {#next-generation-approaches}

The EVOKE trial failures haven't ended GLP-1 research in neurodegeneration -- they've redirected it. Several new directions are being explored.

Dual and Triple Agonists With Better Brain Penetration

Current GLP-1 agonists on the market have long half-lives in the blood but don't readily cross the blood-brain barrier in large amounts. Newer dual GLP-1/GIP receptor agonists (like tirzepatide) and triple agonists (like retatrutide) have been engineered to cross the BBB more easily. In animal models, these multi-agonists show improved neuroprotection compared to single-agonist drugs (CNS Drugs, 2025).

Prevention vs. Treatment

The most important conceptual shift coming out of the EVOKE results is the distinction between preventing neurodegeneration and treating it once it's established. Multiple studies have shown that GLP-1 agonist users develop dementia at lower rates, but the clinical trials tested treatment of existing disease. In one pooled analysis, people taking semaglutide or liraglutide were less than half as likely to develop dementia compared to those taking neither drug (ALZFORUM, 2025).

Stopping a neurodegenerative process once it has started may be fundamentally different from preventing it from beginning. Future trials may need to focus on at-risk populations (people with diabetes, obesity, or genetic risk factors for Alzheimer's) before cognitive symptoms appear.

Other Neurological Applications

The anti-inflammatory mechanisms of GLP-1 agonists have researchers looking beyond Alzheimer's and Parkinson's. Conditions being explored include:

  • Multiple sclerosis
  • Amyotrophic lateral sclerosis (ALS)
  • Frontotemporal dementia
  • Huntington's disease
  • Lewy body dementia

Each of these shares the common feature of chronic neuroinflammation driving disease progression (Inflammation Research, 2025).

Neuropeptide Connections

The brain's own peptide signaling systems -- including neuropeptides like humanin and MOTS-c from mitochondria, and nootropic peptides like semax and selank -- share overlapping protective mechanisms with GLP-1 signaling. Understanding how these different peptide systems interact in the brain may eventually lead to combination approaches for neuroprotection.

FAQ {#faq}

Did semaglutide fail for Alzheimer's?

In the EVOKE and EVOKE+ trials, oral semaglutide did not slow cognitive or functional decline in patients with early-stage Alzheimer's disease. The drug failed to meet its primary endpoints. However, it did show some positive signals in Alzheimer's-related biomarkers (tau proteins, neuroinflammation markers) measured in cerebrospinal fluid. Many researchers believe GLP-1 agonists may work better for prevention than treatment of established disease.

Should people take GLP-1 agonists to prevent Alzheimer's?

There is no current recommendation to use GLP-1 agonists specifically for dementia prevention. The epidemiological evidence is encouraging but observational, and the clinical trials for treatment have been negative. If you're already prescribed a GLP-1 agonist for diabetes or obesity, the potential brain benefits are a reasonable bonus to keep in mind, but these drugs shouldn't be taken for neurological purposes alone based on current evidence.

What about lixisenatide for Parkinson's?

The LIXIPARK trial showed that lixisenatide prevented motor disability worsening over 12 months in early Parkinson's disease, which was a positive signal. However, the trial was small (156 patients), and secondary measures didn't confirm the finding. The study investigators cautioned against off-label use until larger trials validate the results. A large phase 3 trial of exenatide for Parkinson's did not show benefit.

How do GLP-1 agonists compare to existing Alzheimer's drugs?

Existing Alzheimer's drugs like anti-amyloid antibodies (lecanemab, donanemab) target amyloid plaques directly and have shown modest but statistically significant slowing of decline. GLP-1 agonists target different mechanisms (inflammation, insulin signaling, energy metabolism). They are not competitors to anti-amyloid drugs -- they may eventually be used alongside them in combination approaches targeting multiple disease pathways simultaneously.

Do the cardiovascular benefits of GLP-1 agonists contribute to brain protection?

Almost certainly, to some degree. Stroke is a major risk factor for vascular dementia, and GLP-1 agonists reduce stroke risk by 13-15% across meta-analyses. Improved blood flow, reduced atherosclerosis, and better metabolic health all support brain function. Whether GLP-1 agonists also have direct neuroprotective effects independent of cardiovascular improvement is one of the key unanswered questions.

Are there GLP-1 agonists specifically designed for brain diseases?

Not yet approved, but researchers are developing GLP-1 agonists and dual/triple agonists specifically engineered to better cross the blood-brain barrier. These next-generation compounds show improved neuroprotection in animal models and represent the most promising direction for future clinical trials.

The Bottom Line {#the-bottom-line}

The GLP-1 agonist neurodegeneration story is a case study in the gap between biological plausibility and clinical proof.

On one side: GLP-1 receptors are widely distributed throughout the brain. Animal models consistently show neuroprotection. Multiple epidemiological studies from different countries show that people taking GLP-1 agonists develop dementia at significantly lower rates. The biological mechanisms -- anti-inflammatory effects, restored insulin signaling, amyloid reduction, synaptic protection -- make biological sense.

On the other side: the two largest clinical trials (EVOKE and EVOKE+) showed no benefit for treating established Alzheimer's disease. The phase 3 exenatide trial showed no benefit in Parkinson's. The one positive Parkinson's trial (lixisenatide) was small and had methodological concerns.

The emerging consensus is that GLP-1 agonists may have real neuroprotective potential, but that potential may be limited to prevention and very early intervention -- before neurodegeneration has advanced to the point of clinical symptoms. Reversing or even slowing an established degenerative process appears to be a fundamentally different challenge than preventing one from starting.

For patients currently taking GLP-1 agonists for diabetes or obesity, the brain protection signals are an encouraging secondary benefit worth monitoring. For the field of neurodegeneration research, the next chapter will depend on: (1) next-generation agonists with better brain penetration, (2) prevention trials in at-risk populations, and (3) a clearer understanding of which patients, at which stage, might benefit most.

The science isn't finished. But the simplest version of the headlines -- "Ozempic cures Alzheimer's" -- was always too good to be true.

References {#references}

  1. Holscher C. "The Neuroprotective Effects of Glucagon-Like Peptide 1 in Alzheimer's and Parkinson's Disease: An In-Depth Review." Frontiers in Neuroscience, 2022.

  2. Rhea EM, et al. "Brain Endothelial Cells Regulate Glucagon-Like Peptide 1 Entry Into the Brain via a Receptor-Mediated Process." Frontiers in Physiology, 2020.

  3. Edison P, et al. "Liraglutide in Mild to Moderate Alzheimer's Disease: A Phase 2b Clinical Trial." Nature Medicine, 2025. (ELAD trial)

  4. Novo Nordisk. "EVOKE and EVOKE+: Design of Two Large-Scale Phase 3 Studies Evaluating Semaglutide in Early-Stage Alzheimer's Disease." Alzheimer's Research & Therapy, 2024.

  5. Meissner WG, et al. "Trial of Lixisenatide in Early Parkinson's Disease." New England Journal of Medicine, 2024. (LIXIPARK trial)

  6. Norgaard CH, et al. "Treatment with GLP-1 Receptor Agonists and Incidence of Dementia: Data from Pooled Double-Blind Randomized Controlled Trials and Nationwide Disease and Prescription Registers." PubMed, 2022.

  7. Wium-Andersen IK, et al. "Comparative Effectiveness of GLP-1 Agonists, DPP-4 Inhibitors, and Sulfonylureas on the Risk of Dementia." eClinicalMedicine (The Lancet), 2024.

  8. Zhang Z, et al. "Exploring the Neuroprotective Role of GLP-1 Agonists Against Alzheimer's Disease: Real-World Evidence from a Propensity-Matched Cohort." PMC, 2025.

  9. Holscher C. "Incretin Hormones GLP-1 and GIP Normalize Energy Utilization and Reduce Inflammation in the Brain in Alzheimer's Disease and Parkinson's Disease." CNS Drugs, 2025.

  10. Nowell J, et al. "Repurposing Glucagon-Like Peptide-1 Receptor Agonists for the Treatment of Neurodegenerative Disorders." Nature Aging, 2025.

  11. De Giorgi R, et al. "Glucagon-Like Peptide-1 Medicines in Neurological and Psychiatric Disorders." Cell Reports Medicine, 2025.

  12. Tao J, et al. "Targeting Neuroinflammation in Neurodegenerative Disorders: The Emerging Potential of Semaglutide." Inflammation Research, 2025.

  13. Lam BQ, et al. "GLP-1 Receptor Agonists and Reduced Dementia Risk: Real-World Evidence Stacks Up." British Journal of Clinical Pharmacology, 2025.

  14. Li L, et al. "GLP-1 Receptor Agonists in Alzheimer's and Parkinson's Disease: Endocrine Pathways, Clinical Evidence, and Future Directions." Frontiers in Endocrinology, 2025.

  15. Alzheimer's Association. "GLP-1s and Alzheimer's: What You Need to Know." alz.org, 2025.

  16. Alzheimer's Drug Discovery Foundation. "Readout of Phase 3 Semaglutide Trials Marks Critical Moment in Alzheimer's Research." ADDF, 2025.

  17. BrightFocus Foundation. "How GLP-1s Could Transform Alzheimer's Treatment." BrightFocus, 2025.