We were glad to attend AD/PD 2026 and share our latest scientific posters on advancing preclinical neurobiology research.
March 17 - 21, 2026 | Copenhagen, Denmark
Join Taconic Biosciences at AD/PD 2026: Advances in Science & Therapy
Taconic Biosciences is excited to attend AD/PD 2026, where leaders in the field will gather to explore groundbreaking research and innovative treatments for Alzheimer's and Parkinson's Disease.
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Taconic’s Neuroscience Model Portfolio
Taconic empowers neuroscience research with clinically relevant models and services that align closely with human biology, helping scientists generate more predictive insights for therapeutic development.
With ready-to-use cohorts, expert breeding, and global collaborations, researchers can accelerate project timelines while accessing one of the world’s largest model libraries. Every offering is designed to support precision approaches, reproducibility, and the 3R’s, ensuring meaningful scientific progress with responsible use of animals.
Learn more about our full products and services supporting Neuroscience Research
Taconic offers models across a wide range of neuroscience indications, including:
Advance therapeutic discovery with models that capture both early and late drivers of Alzheimer’s, supporting more predictive and translational outcomes. Taconic offers familial and sporadic AD models, including ARTE10 and humanized APOE lines, with aged cohorts available to shorten study timelines.
Accelerate biomarker validation and treatment development with models that reflect key genetic and mechanistic pathways in PD. Taconic’s portfolio includes mutation-based and conditional models, developed in collaboration with The Michael J. Fox Foundation.
Scientific Posters
In Collaboration with Transpharmation
Behaviour and Biomarker Changes in an APP/PS1 Mouse (ARTE10) Model Reveal Translational Potential for Alzheimer’s Disease and Mood-Related Comorbidities
Authors: Laura Griffin, PhD & Moriah Jacobson, PhD
Aims: Alzheimer’s disease (AD) involves progressive cognitive decline and hallmark pathology, including amyloidβ (Aβ) plaques. Patients show prodromal co-morbidities such as anxiety and agitation. ARTE10 transgenic mice co-express human APP and PS1 mutations linked to familial AD and develop robust Aβ pathology. We aimed to comprehensively characterize ARTE10 mice for prodromal and disease-state behavioural phenotypes and biomarkers.
Methods: 5-month (N=16 WT, N=13 Homozygous (HM) ARTE10) and 10-month (N=16 WT, N=16 HM ARTE10) male mice were tested. Behavioural domains were assessed: mood: nest building, anxiety: canopy test, hyperactivity/agitation: running wheel, sensory-motor gating: pre-pulse inhibition, cognition: Y maze and Morris Water maze (MWM), motor function: rotarod. Plasma, CSF and brain samples were collected to evaluate NfL and amyloid levels using the MesoScale Discovery platform.
Results: Canopy testing showed increased anxiety-like behaviour in HM ARTE10 mice, with reduced open-zone distance (p=0.0086) and less edge-looking (p=0.0452) at 5 months. By 10 months, both measures progressed and remained significant (p<0.0001;p<0.0001). Nest building indicated persistent mood disturbances (5M:p=0.0006;10M:p<0.0001), and running wheels showed consistent hyperactivity (5M:p=0.0233;10M:p=0.0201). Spatial working memory deficits emerged only at 10 months in the Y maze (p=0.0039) and MWM (p=0.0429). Biomarkers showed elevated Aβ42/40 in hippocampus (p=0.015) and cortex (p<0.0001) at 5 months, with greater amyloid at 10 months (p<0.0001). NfL increased in cortex (p=0.0016) and trended in CSF (p=0.06) at 5 months, rising further at 10 months (cortex:p=0.0004,CSF:p=0.0037).
Conclusions: The ARTE10 mouse model exhibits prodromal behavioural phenotypes related to AD, pronounced amyloid pathology and early detectable biomarkers. Several phenotypes and biomarkers progress with age. These features support the strong translational potential of this model to advance therapeutic developments for AD, including those related to core pathology and comorbid symptoms that are not currently managed by approved treatments.
In Collaboration with Gubra
High-Throughput 3D Whole-Brain Imaging Reveals Sex-Dependent Parenchymal and Vascular Amyloid Plaque Architecture in a Standard Mouse Model of Alzheimer’s Disease
Authors: Laura Griffin, PhD
Aims: Both age and sex are key modulators in Alzheimer’s disease (AD) pathology, and cerebral amyloid angiopathy (CAA) is increasingly recognized as an important contributor to the progression of AD. To enable the development of more effective interventions, preclinical studies should incorporate these factors in the evaluation of drug candidates. In this study, we applied light-sheet fluorescence microscopy (LSFM) combined with AI-enabled image analysis to compare age-dependent changes in whole-brain plaque architecture between female and male transgenic AD mice.
Methods: Intact brains from 15-, 30-, and 42-week-old female and male APP/PS1 transgenic (ARTE10) mice, along with 30-week-old male wild-type controls, were co-stained for amyloid plaques (anti-human Aβ) and vasculature (anti-mouse CD31+podocalyxin), cleared, and imaged using light-sheet fluorescence microscopy. Deep learning-based image analysis was established to for whole-brain segmentation, anatomical mapping, and quantification of parenchymal and vasculature-associated plaques in more than 800 individual mouse brain regions.
Results: ARTE10 mice exhibited age- and sex-dependent differences in whole-brain amyloid plaque architecture. While both sexes showed age-related increases in plaque load across the cortex, hippocampus, and neighbouring regions, disease progression was faster in females. Cortical plaque expansion followed an age-dependent gradient, extending from deeper to more superficial layers. Parenchymal plaques were detectable by 15 weeks in both sexes, whereas vascular plaques appeared more consistently at 30 and 42 weeks, indicating a delayed onset of CAA in this model.
Conclusions: We established a framework for high-throughput, quantitative 3D whole-brain imaging to assess plaque load in a standard APP/PS1 transgenic mouse model of AD. Our findings highlight the necessity of accounting for both sex and age as critical variables when designing intervention studies, and profiling drug candidates in mouse models of AD and CAA.
Authors
Laura Griffin, PhD 
Associate Director, Cardiometabolic Portfolio
Dr. Laura Griffin has been working with preclinical models for a decade and is experienced in choosing appropriate models for various research applications. She obtained her PhD in Food Science and Technology at Virginia Tech, where she focused on the mechanisms by which dietary bioactive compounds influence the onset of metabolic syndrome using preclinical models. As a postdoctoral fellow at the Plants for Human Health Institute, her research shifted to focus on the impact of the gut microbiome on the metabolism of bioactive compounds. In addition to her expertise in metabolic diseases in preclinical models, Dr. Griffin is also versed in laboratory animal diets and their usage in preclinical applications.
Moriah Jacobson, PhD
Associate Director, Scientific Solutions
Dr. Moriah Jacobson joined Taconic Biosciences as a Field Applications Scientist in October 2020, and is now Associate Director, Scientific Solutions. She has deep expertise in the development, execution, and review of translational rodent studies. She obtained her Ph.D. in Integrative Neuroscience from Stony Brook University, where she discovered novel biomarkers for several models of chronic stress and chemotherapy-induced cognitive impairment and peripheral neuropathy. She then completed her postdoctoral research at Uniformed Services University where she studied novel rapid acting antidepressant drugs targeting kappa opioid receptors.
Learn from Experience
Our team brings extensive expertise in managing animal models across diverse research areas. By sharing practical insights into model selection, colony management, and welfare-focused strategies, we aim to help researchers design studies that are both efficient and responsible.
Sarah Sterlace, PhD
Senior Director, Portfolio Management Neurobiology and Rare Disease
Dr. Sarah Sterlace joined Taconic in 2024 and is currently Director of Portfolio Management focusing on Neurobiology and Rare Disease. Sarah has more than 10 years of experience in drug discovery and life sciences support with an emphasis in emerging technologies and customer-focused solutions for advancing translational research.
Jens Christian Laursen, MS
Director, Scientific Product Management
Jens Christian holds a B.Sc. in medicine and a M.Sc. in translational medicine from Aalborg University, Denmark. After completing his M.Sc. degree, Jens Christian was engaged in studying neuropharmacology and the peripheral nervous system, specifically related to the study of nociception and craniofacial pain. The research was focused on in vitro and in vivo studies and he authored and co-authored on these topics over the course of 3 years. Jens Christian joined Taconic in 2014 as a Project Manager and since then became a Scientific Program Manager and today he oversees the Global Scientific Program Management team related to Custom Colony Management and related services in the pre-clinical space.
Ditte Olsen, PhD
Scientific Solutions Consultant
Dr. Ditte Olsen received her Master of Science in Molecular Biology from Aarhus University, Denmark and earned her industrial PhD in Neuroscience from Aarhus University and Lundbeck. During her PhD, Ditte studied the dopaminergic system in various transgenic animal models.
During her postdoctoral training, her focus changed to the field of cardiovascular disorders. Following her postdoctoral training, she joined a biotech company where her focus was on preclinical research using small molecules to reduce high cholesterol levels. Ditte brings nearly 15 years of in vivo research experience to her role as a Scientific Solutions Consultant at Taconic.
Jens-Ole Bock
Client Relationship Manager
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