EAN 2025 Highlights: Advances across dementia, headache, movement disorders, cerebrovascular and neuromuscular diseases

© 2025 European Academy of Neurology

The 11th Congress of the European Academy of Neurology (EAN) delivered ground-breaking insights across neurology, showcasing how precision medicine is reshaping clinical practice. Taken from the EAN Highlights and Breaking news session presented 24 June 2025 (PLEN03), touchNEUROLOGY summarizes the key highlights across dementia, headache, movement disorders, cerebrovascular and neuromuscular diseases.

Dementia: Biomarkers informing early diagnosis

Headache: Biomarkers and novel treatments

Movement disorders: From biomarkers to devices

Cerebrovascular diseases: Data driving decisions

Neuromuscular diseases: A therapeutic revolution

Several key studies at EAN 2025 focused on the role of metabolic dysfunction and biomarkers in Alzheimer’s disease (AD). A retrospective single-centre study presented by Prof. Bianca Gumina valuated the triglyceride–glucose (TyG) index in non-diabetic patients with AD. Elevated TyG levels were significantly associated with accelerated cognitive decline in mild cognitive impairment (MCI) due to AD, particularly in APOE4 carriers. This association was not observed in other neurodegenerative disorders, suggesting insulin resistance may be a specific driver of early AD progression.^1,2,3

Another study examined cerebrospinal fluid (CSF) synaptic markers, neurogranin, SNAP-25 and CAP-2, as well as inflammatory biomarkers. CAP-2 showed the strongest correlation with neuroinflammation and neurodegeneration, but not with amyloid burden, suggesting a synaptic compensatory mechanism independent of amyloid pathology.^⁴

In addition, MRI studies revealed early blood–brain barrier (BBB) dysfunction in the basal forebrain, a region implicated early in AD. Astrocyte markers, including GFAP and lactate, correlated with BBB impairment in APOE4-positive individuals.⁵

Transcranial magnetic stimulation (TMS) studies led by Dr F. Massa et al. revealed early cholinergic deficits in individuals with subjective cognitive decline, MCI and AD. Coupled FDG-PET and CSF neuronal pentraxin-2 (NPTX2) studies indicated serotonergic dysfunction that correlated with disease severity.⁶

A pivotal study from the Danish Headache Centre showed that pituitary adenylate cyclase-activating polypeptide (PACAP)-38 levels were elevated in both active and remission phases of migraine, independently of calcitonin gene-related peptide (CGRP) levels. This positions PACAP as a potential biomarker, though further validation is required.⁷

In an Italian study presented by Dr Marina Romozzi, CGRP levels in tear fluid were significantly elevated in migraine patients compared with controls and reduced after anti-CGRP therapy, suggesting tear fluid as a non-invasive diagnostic matrix.⁸

Dr Simone Braca’s investigation into liraglutide, a glucagon-like peptide-1 (GLP-1) receptor agonist, demonstrated significant reductions in headache frequency among patients with obesity and migraine, independent of weight loss. Randomized controlled trials are warranted to confirm these findings.⁹

The RESOLUTION trial, presented by Prof. Stewart Tepper, showed that eptinezumab, combined with patient education, led to sustained improvements in quality of life, reduced headache burden and improved work productivity in individuals with chronic migraine and medication-overuse headache.¹⁰

Final results from the 24-month PEARL study, presented by Prof. Messoud Ashina, confirmed the long-term safety and tolerability of fremanezumab for migraine prevention. Among 1,140 patients with episodic or chronic migraine, 56.5% achieved a ≥50% reduction in monthly migraine days. Adverse events were reported by 56.3%, most commonly mild injection site or gastrointestinal issues. Serious drug-related adverse events were rare (0.4%).¹¹

Genetic studies presented at EAN 2025 highlighted the roles of LRRK2 and GBA variants in modulating Parkinson’s disease (PD) risk and progression, prompting genetically informed clinical trials and new disease-modifying strategies.^12,13

Advances in device-assisted therapies were also showcased. Subcutaneous foslevodopa/foscarbidopa was found to reduce motor fluctuations in PD. Additionally, adaptive deep brain stimulation (aDBS) using real-time feedback loops is approaching clinical use.¹⁴

The PASADENA (phase II) and PADOVA (phase IIb) trials evaluating prasinezumab, an anti-alpha-synuclein monoclonal antibody for early-stage PD, did not meet primary endpoints. However, secondary analyses showed encouraging trends, particularly in subgroups, with a consistent safety profile supporting advancement into phase III.^15,16

© 2025 European Academy of Neurology

The TenCRAOS trial (NCT03197194) examined tenecteplase for central retinal artery occlusion but found no significant benefit in visual outcomes. Additionally, an increased rate of serious adverse events, including one treatment-related death, raised safety concerns.¹⁷

In Catalonia, a regional study presented by Dr J. Mayol demonstrated that deploying endovascular thrombectomy (EVT) in primary stroke centres reduced time to reperfusion without compromising safety. Training neurologists to perform EVT helped overcome geographic and specialist shortages.¹⁹

The DECOMPRESS 2 study assessed anticoagulation restart timing after decompressive surgery for cerebral venous sinus thrombosis. Restarting within 24 hours did not significantly affect risks of rebleeding or thrombosis, offering practical guidance.²⁰

A Milanese study applying the Boston criteria 2.0 to cerebral amyloid angiopathy (CAA) found that lower CSF Aβ42 correlated with haemorrhagic history. Although CAA diagnoses increased among patients with AD, the clinical implications of Boston 2.0 remain under review.²¹

A meta-analysis of 16 trials (e.g. NCT03889249) confirmed tenecteplase is associated with superior functional outcomes compared with alteplase in ischaemic stroke, with similar safety profiles, suggesting a shift in standard of care.²²

© 2025 European Academy of Neurology Prof. Elena Moro, EAN President

Gene and molecular therapies featured prominently in neuromuscular disease sessions. Dr Ting Chang presented data on low-dose BCMA/CD19 dual chimeric antigen receptor (CAR) T cells for refractory myasthenia gravis, which yielded rapid and durable responses beyond conventional immunotherapy.²³

In Duchenne muscular dystrophy (DMD), delandistrogene moxeparvovec received accelerated approval based on microdystrophin expression and improved functional outcomes.²⁴

Novel immunotherapies such as efgartigimod²⁴ and empasiprubart (ENVIGORATE phase III trial, NCT06920004) are advancing treatment options in chronic inflammatory demyelinating polyneuropathy (CIDP) and nodal–paranodal neuropathies.²⁵

Finally, a German single-centre study involving 125 people with multiple sclerosis found that serum neurofilament light chain (sNfL) levels may indicate response to monoclonal antibodies. Extended-interval dosing did not increase sNfL, suggesting a safe de-escalation strategy.²⁶

EAN 2025 highlighted the rapid evolution of precision neurology. Advances in biomarkers, targeted therapies and device innovations are transforming clinical approaches across dementia, headache, movement, cerebrovascular and neuromuscular diseases. The integration of precision medicine continues to reshape neurological care.

Resources: The full conference proceedings and abstract book is available as a special supplement issue: European Journal of Neurology, Volume 32, Issue S1 (2025).

Disclosures: This content has been created based on the EAN Highlights and Breaking news session presented 24 June 2025 (PLEN03). This content has been developed independently by Touch Medical Media for touchNEUROLOGY. No funding was received in the publication of this article.

References:

1. Gumina B, Galli A, Tolassi C. The triglyceride–glucose index as predictor of cognitive decline in Alzheimer’s spectrum disorders. Abstract #OPR-066. Presented at: EAN 2025.

2. Padovani A, Galli A, Bazzoli E, et al. The role of insulin resistance and APOE genotype on blood–brain barrier integrity in Alzheimer’s disease. Alzheimers Dement. 2025. doi:10.1002/alz.14556

3. EurekaAlert. Simple blood test predicts cognitive decline in Alzheimer’s patients, new study shows. Available at: https://www.eurekalert.org/news-releases/1087799 (accessed 5 July 2025).

4. Martinuzzo C, Trasciatti C, Pilotto A, et al. CSF synaptic biomarkers negatively correlate with disease duration: New insights into Alzheimer’s disease synaptopathy. Abstract #EPO-180. Presented at: EAN 2025.

5. Lerch O, Kala D, Nedelska Z, Hadzic H, et al. DCE-MRI reveals impaired blood brain barrier in basal forebrain region in patients with Alzheimer’s disease. Abstract #EPO-357. Presented at: EAN 2025.

6. Massa F, Orso B, Garbarino S, et al. Serotonergic receptor maps overlap with cortical metabolism changes and CSF NPTX2 in prodromal Alzheimer’s disease. Abstract #EPO-182. Presented at: EAN 2025.

7. Amin FM, Asghar MS, Guo S, et al. PACAP38-induced migraine attacks are independent of CGRP signaling: A randomized controlled trial. J Headache Pain. 2025;26:41. doi:10.1186/s10194-025-02022-2

8. Romozzi M, Di Nardo L, Trigila V, et al. CGRP increase in tear fluid of migraine patients is reversed by anti-CGRP monoclonal antibodies. Abstract #OPR-011. Presented at: EAN 2025.

9. Braca S, Russo C, Stornaiuolo A, et al. GLP-1R agonists for the treatment of migraine: A pilot prospective observational study. Abstract #OPR-012. Presented at: EAN 2025.

10. Tepper S, Schytz H, Jensen R, et al. Eptinezumab reduced disease burden in chronic migraine and medication-overuse headache: Secondary RESOLUTION trial data. Abstract #EPO-236. Presented at: EAN 2025.

11. Ashina M, Mitsikostas D, Amin F, et al. Real-world safety and tolerability of fremanezumab in migraine prevention: Final outcomes of the PEARL study. Abstract #EPO-063. Presented at: EAN 2025.

12. Roque MM, Valadas A, Coelho M, et al. Patient-based retrospective reporting of motor and nonmotor symptoms in LRRK2-related versus idiopathic Parkinson’s disease. Abstract #EPO-263. Presented at: EAN 2025.

13. Lüth T, Laabs B, Sendel S, et al. The age at onset of LRRK2-related Parkinson’s disease across ancestries and countries of origin. Abstract #EPO-670. Presented at: EAN 2025.

14. Ciaramaglia O, De Micco R, D’Anna M, et al. Effects of subcutaneous foslevodopa–foscarbidopa on motor and nonmotor symptoms in Parkinson’s disease. Abstract #EPO-444. Presented at: EAN 2025.

15. Poewe W, Bloem BR, Goetz CG, et al. Efficacy and safety of prasinezumab in early Parkinson’s disease (PASADENA): A randomised, double-blind, placebo-controlled, multicentre, phase 2 trial. Eur J Neurol. 2025. doi:10.1111/ene.70263

16. EAN Congress 2025. PADOVA trial open-label extension update. Available at: https://www.eanvirtualcongress.org/ean/ean2025/en-GB/presentation/529535 (accessed 7 July 2025).

17. BusinessWire. Prothena’s partner Roche to advance prasinezumab into phase III development for early-stage Parkinson’s disease. Available at: https://www.businesswire.com/news/home/20250615297680/en/ (accessed 7 July 2025).

18. Darsalia V, Kristensson J, Nyström T, et al. Tenecteplase versus alteplase for acute ischemic stroke: Meta-analysis of randomised controlled trials. Eur Stroke J. 2025. doi:10.1177/23969873251344199

19. Mayol J, García-Tornel Á, Rodrigo-Gisbert M, et al. Clinical impact of endovascular treatment implementation in primary stroke centres of Catalonia. Abstract #OPR-021. Presented at: EAN 2025.

20. Taveira MC, Aaron S, Ferreira JM, et al. Timing of anticoagulation following decompressive surgery for cerebral vein and sinus thrombosis: An observational study. Abstract #OPR-022. Presented at: EAN 2025.

21. De Franco V, Mazzacane F, Prodi E, et al. Cerebral amyloid angiopathy prevalence in Alzheimer’s disease according to different Boston criteria versions. Abstract #EPO-134. Presented at: EAN 2025.

22. Ifzal M, Afzal S, Rizvi S, et al. Tenecteplase administration after the usual treatment window in acute ischaemic stroke: A meta-analysis. Abstract #EPO-204. Presented at: EAN 2025.

23. Chang T, Ruan Z, Li Y, et al. BCMA/CD19 dual CAR-T cells for refractory myasthenia gravis. Abstract #OPR-056. Presented at: EAN 2025.

24. Cornblath D, Wilson J, Baquié M, et al. Immunoglobulin versus efgartigimod: Indirect comparisons in chronic inflammatory demyelinating polyneuropathy. Abstract #EPO-140. Presented at: EAN 2025.

25. Cornblath D, Wilson J, Baquié M, et al. ENVIGORATE phase III trial of empasiprubart in CIDP. Abstract #EPO-140. Presented at: EAN 2025.

26. Konitsioti A, Schweitzer F, Johannis W, et al. Serum neurofilament light chain as a biomarker for treatment efficacy of extended-interval dosing in multiple sclerosis. Abstract #EPR-054. Presented at: EAN 2025.

Cite: EAN 2025 Highlights: Advances across dementia, headache, movement disorders, cerebrovascular and neuromuscular diseases. touchNEUROLOGY. 10 July 2025.

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