AD/PD™ (Alzheimer's & Parkinson's Diseases Conference) is described as the premier annual event in the field of neurodegenerative diseases. Founded in 1985, AD/PD has evolved from a focused meeting on Alzheimer's disease to a comprehensive conference bringing together researchers and clinicians working on both Alzheimer's disease and Parkinson's disease.
The integrated approach distinguishes AD/PD from single-disease conferences, enabling researchers to explore common molecular pathways, shared therapeutic approaches, and biomarker overlap between these two most common neurodegenerative conditions. This unique positioning has made AD/PD one of the most influential meetings in the neurodegeneration field.
| Item |
Details |
| Dates |
March 17-21, 2026 |
| Location |
Copenhagen, Denmark — Bella Center Copenhagen |
| Organizer |
Kenes Group |
| Website |
adpd.kenes.com |
The Alzheimer's track covers the full spectrum of AD research:
- Amyloid Biology: Amyloid-beta generation, aggregation, and toxicity mechanisms
- Tau Pathology: Tau phosphorylation, propagation, and tau-targeted therapies
- Neuroinflammation: Microglial activation, complement system, and inflammatory pathways
- Neurodegeneration: Synaptic loss, neuronal death mechanisms
- Biomarkers: Fluid and imaging biomarkers for diagnosis and trial enrichment
- Clinical Trials: Disease-modifying therapies and symptomatic treatments
The Parkinson's track addresses all aspects of PD:
- Alpha-Synuclein: Aggregation, propagation, and therapeutic targeting
- Lewy Body Pathology: Formation, composition, and disease relevance
- Mitochondrial Dysfunction: PINK1, Parkin, and mitophagy pathways
- Neuroinflammation: Microglial activation in PD pathogenesis
- Genetic Risk Factors: LRRK2, GBA, SNCA, and other genetic contributors
- Motor Complications: Levodopa-induced dyskinesias and motor fluctuations
A key strength of AD/PD is exploring shared mechanisms:
- Protein Aggregation: Common mechanisms in AD (amyloid/tau) and PD (alpha-synuclein)
- Neuroinflammation: Shared inflammatory pathways across neurodegenerative diseases
- Biomarker Overlap: Common fluid and imaging biomarkers
- Therapeutic Approaches: Targeting common pathways (e.g., neuroprotection)
- Aging Mechanisms: Role of aging in neurodegeneration
- Keynote Lectures: Major presentations by field leaders
- Symposia: Focused sessions on specific topics
- Oral Communications: Selected abstract presentations
- Poster Sessions: Interactive poster presentations
- Workshops: Hands-on educational sessions
- Meet-the-Expert: Informal Q&A sessions with leading researchers
- Morning: Symposia, workshops
- Midday: Poster sessions, lunch meetings
- Afternoon: Oral communications, keynotes
- Evening: Social events, networking
The 2026 conference featured the following key session types:
Keynote Sessions
- Opening Keynote: Future of Neurodegeneration Research
- Amyloid Hypothesis: Where Do We Stand?
- Tau Pathology: From Basic Science to Therapy
- Alpha-Synuclein: The Central Player
- Closing Vision 2030
Plenary Symposia
- Neuroinflammation: Common Ground Across Diseases
- Biomarkers Across Diseases
- Genetics and Precision Medicine
- Clinical Trial Design Innovations
Oral Abstract Sessions
- Parallel sessions across all topics
- Young Investigator presentations
Poster Sessions
- Five themed poster sessions throughout the week
- Interactive Q&A with presenting authors
The 2026 conference returns to Copenhagen, a city renowned for its research excellence:
- Scandinavia's largest conference center — over 143,000 m² of exhibition space
- Address: Center Blvd 5, 2300 Copenhagen S, Denmark
- State-of-the-art facilities with advanced AV technology
- Excellent accessibility — Copenhagen Airport (CPH) is 20 minutes away via metro
- Sustainable venue practices — LEED certified facility
- Multiple exhibition halls and parallel session rooms
- On-site registration and industry exhibition space
- Capacity: Up to 18,000 delegates across all halls
- Metro M1 line: Direct to Bella Center station (20 minutes)
- Taxi: Approximately 15-20 minutes
- Train: 4-minute walk from Terminal 3 to M1 line
- Metro M1 line: 15 minutes directly to Bella Center station
- Bus: Lines 30 and 34 connect to Bella Center
- Øresund Bridge: 35 minutes by train via Malmö Central
- The conference is easily accessible from throughout Scandinavia
- Public Transport Zone: The venue is in Zone 4, covered by standard passes
- Copenhagen Card: Unlimited public transport + entry to attractions
- Bike Rental: Copenhagen's renowned bike-share system available at the venue
- Hotels: Many within walking distance — book early for discounts
- Best time to visit: March can be chilly (5-10°C), bring layers
- Currency: Danish Krone (DKK), many places accept EUR
- Language: English widely spoken
- Electricity: Type C/F outlets (220V)
AD/PD has played a crucial role in advancing neurodegenerative disease research:
- 1985: First AD/PD conference held in Zurich
- 2000s: Expanded to include Parkinson's disease
- 2010s: Growth of biomarker-focused sessions
- 2020s: Virtual participation options, record attendance
- 2026: Return to Copenhagen with expanded programming
- First real-world effectiveness data for anti-amyloid therapies (Leqembi, Donanemab)
- Advancing tau PET standardization and clinical utility
- Seed amplification assays for alpha-synuclein now in clinical use
- LRRK2 inhibitor pivotal trial results
- Blood-based biomarkers (p-tau217, p-tau231) transforming trial design
- Novel neuroprotective strategies entering clinical trials
At AD/PD 2026 in Copenhagen, researchers presented early PET imaging studies showing that a new generation of alpha-synuclein PET tracers has entered human testing. These tracers are being evaluated in people with different synucleinopathies (Parkinson's disease, Dementia with Lewy Bodies, Multiple System Atrophy). This represents a major milestone for synucleinopathy diagnostics, as alpha-synuclein PET has historically lagged behind amyloid and tau imaging. Once validated, these tracers will enable differential diagnosis of parkinsonisms, disease staging, and clinical trial enrollment criteria for alpha-synuclein-targeted therapies.
In Copenhagen at AD/PD 2026, Henrik Zetterberg (University of Gothenburg, UCL) expounded on the next areas of focus in ADRD biomarker research and development. His mantra — heterogeneity, heterogeneity, heterogeneity — emphasized that Alzheimer's and related dementias are not a single disease but a spectrum of conditions with diverse molecular drivers, clinical presentations, and treatment responses. Key themes from his talk included:
- Patient stratification based on fluid and imaging biomarkers
- Subtype-specific therapeutic approaches targeting distinct molecular pathways
- Precision medicine frameworks matching patients to targeted interventions
- Biomarker-driven trial designs using p-tau217, NfL, and other markers for enrollment
- Cross-disease biomarker overlap between AD, PD, FTD, and other neurodegenerative conditions
Zetterberg's emphasis on heterogeneity aligns with the growing recognition that neurodegenerative diseases require personalized approaches based on molecular phenotyping rather than clinical diagnosis alone.
At AD/PD 2026, AI scientists competed for two $1 million prizes to develop products for Alzheimer's research. The C-BRAIN initiative brought together computational approaches to advance AD diagnosis, prognosis, and therapeutic target identification.
In a plenary session at AD/PD 2026, Bart De Strooper (KU Leuven, UK Dementia Research Institute) offered a vision of successive cellular struggles in Alzheimer's pathophysiology, identifying three key inflection points in the amyloid cascade where therapeutic intervention may be most effective. This framework highlights:
- Early amyloid accumulation as the initiating trigger
- Cellular stress responses as the amplification phase
- Neurodegeneration as the final common pathway
This model suggests that early intervention before the cascade amplifies may be critical for disease modification.
In Chinese and European cohorts, neuronal pentraxin-1 (NPTX1) and neuronal pentraxin receptor (NPTXR) predicted neurodegeneration. These synaptic markers provide a window into synaptic integrity and may serve as early indicators of neuronal vulnerability in Alzheimer's disease.
CSF proteomics revealed that microglia transition from mobilized to dysregulated states as Alzheimer's disease advances. This trajectory reflects the evolving role of neuroinflammation across disease stages — initially protective, then increasingly pathogenic.
An epigenome-wide scan of Alzheimer's brains links phospho- and soluble tau to methylation of oligodendrocyte genes, suggesting a novel mechanism by which tau pathology disrupts white matter integrity and myelination.
- Alpha-synuclein seed amplification assay validation studies
- LRRK2 inhibitor clinical trial results
- Amyloid PET standardization efforts
- Tau PET tracer development
- Novel anti-aggregation compound discovery
- Combined biomarker panels for diagnosis
The AD/PD 2026 conference emphasized several critical themes:
- Lecanemab (Leqembi) and Donanemab demonstrating real-world effectiveness
- Focus shifting to earlier intervention and prevention
- Combination therapy approaches emerging
- Seed amplification transforming diagnosis
- Immunotherapy approaches showing promise
- LRRK2 inhibitor clinical data maturing
- Genetic stratification (LRRK2, GBA, SNCA)
- Subtype-specific therapeutic approaches
- Personalized trial designs
The AD/PD conference is unique in its integration of Alzheimer's and Parkinson's research:
- Protein misfolding and aggregation
- Neuroinflammation across diseases
- Mitochondrial dysfunction
- Synaptic failure
- Cellular senescence
- Shared fluid biomarkers
- Common imaging targets
- Cross-disease validation studies
- Neuroprotective strategies
- Gene therapy platforms
- Immunotherapy approaches
- Cell-based therapies