The winds whipping across the Öresund this March did little to chill the atmosphere inside the Bella Center. As the 20th International Conference on Alzheimer’s and Parkinson’s Diseases (AD/PD™ 2026) unfolded in Copenhagen, the atmosphere was one of hard-won momentum. For years, the field was dominated by the “amyloid cascade” debate, but this year, the spotlight shifted decisively toward the structural and molecular nuances of tau.

AD/PD 2026: By the numbers and on the floor, there was too much to see and do in a week!

The core takeaway from the week? We cannot continue to think of neurodegeneration as a monolith, but as a complex map of cellular vulnerability. The path forward will entail building a precision biotyping framework that understands this nuance.

While Alzheimer’s Disease (AD) involves a mixed 3R/4R tau pathology alongside amyloid-beta, primary tauopathies like Progressive Supranuclear Palsy (PSP) and Corticobasal Degeneration (CBD) are driven by the 4R isoform. These “pure” tau diseases are increasingly seen as the ultimate testing ground for tau-targeting therapies. PSP often suffers from a diagnostic lag, with patients spending years in the Parkinson’s-plus waiting room. AD/PD highlighted several research findings and tools aimed at ending this uncertainty.

Two Standout Oral Sessions

This presentation showcased the diagnostic potential of AI-driven plasma proteomics using a massive dataset from the Global Neurodegeneration Proteomics Consortium (GNPC). The team introduced ProtAIDs-Dx, a deep neural network that utilizes a refined set of approximately 200 plasma proteins to classify major dementia subtypes—including AD, PD, FTD, and ALS—with impressive precision (AUC > 0.8). Beyond simple classification, the model’s probabilistic outputs correlated strongly with APOE status and MMSE scores. Remarkably, its baseline measurements were able to predict longitudinal cognitive decline (AUC of 0.74).

The talk utilized statistical methods to demonstrate how the dataset revealed disease heterogeneity, identifying distinct patient “clusters” that correlate with specific comorbidities. Most significantly for clinical application, the model was successfully validated against the external BioFINDER-2 cohort, where it served as a reliable proxy for invasive biomarkers like CSF ptau217 and neuroimaging markers such as white matter hyperintensity. This shift toward a probabilistic approach highlights a future where a single blood draw, analyzed through the lens of explainable AI, could provide a comprehensive view of a patient’s multi-pathology landscape and projected disease trajectory.

The Phase 1 trial results for NIO752 (NCT04539041), a first-in-class antisense oligonucleotide (ASO) targeting the MAPT gene, represent a landmark moment for primary tauopathy research. The study demonstrated that NIO752 was generally well-tolerated in patients with PSP following intrathecal administration. Most importantly, the trial achieved a significant, dose-dependent reduction in total tau levels within the cerebrospinal fluid, providing the first clinical proof-of-concept for tau lowering in a 4R tauopathy.

The data showed that NIO752 effectively suppresses the production of all tau isoforms at the mRNA level, which is a strategic shift from previous failed antibody trials that targeted only extracellular protein. While the Phase 1 study was primarily powered for safety and pharmacokinetics, the robust biomarker signal has paved the way for an upcoming Phase 3 trial. This approach offers a promising disease-modifying strategy. It tackles the underlying genetic driver of tau aggregation before the protein can misfold and spread through the brain.

Poster Hall Happenings

Beyond the scientific sessions, the heart of the conference was in the poster hall. Our team loved connecting one-on-one with researchers among the 1,800+ exhibits, gaining deeper insight into the incredible work driving their individual programs. Below are very brief highlights from five posters that caught our attention.

This study explored the utility of plasma pTau217, typically an AD marker, within the context of PSP phenotypes (PSP-RS, PSP-P, and PSP-COG). The research identified that the highest levels of pTau217 were found in the PSP-COG phenotype, suggesting a trend toward higher tau burden in cases with prominent cognitive impairment. Furthermore, a lower plasma Aβ42/40 ratio was associated with worse cognitive and functional severity across all phenotypes. These findings suggest that a subset of PSP patients may harbor an AD-like biological profile that accelerates cognitive decline, highlighting the need for multi-biomarker screening to capture the full spectrum of pathology (and often, copathology) in primary tauopathies.

  • The Clinical and Mortality Burden of Progressive Supranuclear Palsy: a Matched Cohort Study (UCB, poster ID 428) Click to view the poster.

In a large-scale matched cohort study using UK primary care data, researchers quantified the staggering impact of PSP on patient longevity and quality of life. The data revealed that individuals with PSP face a 12-fold higher probability of death compared to controls, with a median survival of just 3.9 years following the first recorded symptom. Crucially, the study noted that the clinical burden, including falls, depression, and sleep disorders, precedes the formal diagnosis, often by years. This reinforces the urgent need for earlier diagnostic interventions to manage comorbidities and prepare families for the rapid progression associated with the disease.

  • Vertical and Horizontal Saccades Are Comparably Impaired in Progressive Supranuclear Palsy (Queensland Brain Institute, poster ID 1559)

Challenging the long-standing clinical dogma that vertical saccades are uniquely or disproportionately affected in PSP, this study utilized video-oculography to compare eye movements across PSP, AD, and LBD cohorts. The results demonstrated that while vertical saccades are indeed slower and more interrupted in PSP, horizontal saccades are impaired to a nearly identical degree. The researchers argue that PSP presents a global saccadic impairment rather than a vertical-specific one. This insight could refine diagnostic criteria, shifting the focus from purely vertical gaze palsy to a more comprehensive assessment of overall saccadic velocity and trajectory.

  • The Diagnostic Odyssey and Impact on Quality of Life in People With PSP and CBD (PSPA, poster ID 202)

This poster highlighted the diagnostic odyssey experienced by patients and caregivers, revealing that approximately 60% of people with PSP or CBD are initially misdiagnosed, most commonly with Parkinson’s Disease. While the time spent at the GP level has decreased since 2016, the study identified a new bottleneck: increased waiting times to see a neurologist, with only 44% of respondents being seen within three months of referral. The human cost is significant, with 92% of patients reporting that a loss of independence profoundly affects their daily life. These findings underscore the critical need for better healthcare professional education to close the gap between symptom onset and accurate diagnosis.

Representing an improved therapeutic approach, this poster characterized NIDB-3101, a novel biparatopic antibody designed to target both the R4 domain and the C-terminal of the tau protein. Unlike earlier generations of antibodies, NIDB-3101 demonstrated a high affinity for a broad range of tau species, including monomers, fibrils, and truncated seeds. In cell-based assays, the antibody effectively neutralized tau seeds and inhibited aggregation more efficiently than current benchmark analogs. While initially presented in the context of AD, its ability to bind the 4R-rich microtubule-binding region makes it a potential candidate for future trials in primary tauopathies too.

Onwards From Copenhagen

The Copenhagen spirit was one of profound optimism. The tools are available, the cohorts are organized, and for diseases like primary tauopathies, the silence of the “rare disease” label is finally being replaced by the noise of active, high-stakes science. We look forward to seeing many of these outstanding researchers again soon at Tau Global 2026.