We were glad to attend SfN 2025 and share our latest scientific posters on advancing preclinical neuroscience research. If you missed us at SfN, fill out the form to access our posters.
November 15 – November 19, 2025 | San Diego, California, USA | Booth #2512
Taconic Biosciences at Neuroscience 2025
Taconic offers a diverse portfolio of rodent models and services to support translational neuroscience research across major disease areas. Discover our selection of SfN 2025 posters and neuroscience resources below.
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- Neuroscience Models
- Scientific Posters
- Meet the Team
- Resources
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.
Drive reliable efficacy studies using models that provide measurable, progressive endpoints aligned with disease pathology. Taconic offers ALS models such as the SOD1 rat, which demonstrates hallmark motor neuron degeneration.
Connect human genetics to functional outcomes with models that enable research into behavioral and cognitive changes. Taconic provides copy-number variation models, including lines that represent autism, schizophrenia, and epilepsy drivers.
Gain real-time insights into CNS processes with noninvasive imaging tools that streamline pharmacology and injury research. Taconic offers reporter lines such as GFAP-Luc and CRE-Luc to monitor inflammation and signaling activity.
Scientific Posters
We presented three scientific posters at SfN 2025, including one submitted directly by our team and two developed in collaboration with our scientific partners.
November 16th, 2025, 8:00 a.m. - 12:00 p.m. | History of Neuroscience
Alzheimer's Disease: History of Animal Models for Therapeutic Discovery | Session Number: TKP01
Moriah Jacobson, PhD, Taconic Biosciences
Alzheimer’s disease (AD) is a complex neurodegenerative disorder marked by progressive cognitive decline, amyloid-β (Aβ) plaque accumulation, and neurofibrillary tangles (NFTs). Animal models have been instrumental in advancing our understanding of AD pathology and in developing potential therapies.
First-generation AD models, such as Tg2576 and TgCRND8 mice, overexpressed mutant human APP, leading to robust Aβ plaque deposition. While valuable for studying amyloidosis and testing anti-Aβ compounds, these models lacked NFTs, neuronal loss, and reflected familial AD (FAD), which accounts for <5% of cases. High transgene overexpression also introduced non-physiological phenotypes, limiting their translational relevance.
Second-generation models improved upon these limitations by incorporating multiple FAD mutations, such as ARTE10 (APP/PS1) or 3xTg-AD mice, which presented both amyloid and tau pathology. These models provided a more comprehensive view of AD and enabled studies on amyloid–tau interactions. However, they still relied on overexpression and failed to fully replicate human tauopathy, sporadic AD mechanisms, or consistent neuronal degeneration.
Third-generation models emphasize physiological expression through knock-in strategies (e.g., CRISPR/Cas9) and inclusion of human risk alleles such as APOE4 and TREM2, better capturing sporadic AD pathology. These models show more accurate disease progression, including neuroinflammation, synaptic dysfunction, and neuronal loss. Although more complex and time-intensive to develop, they hold greater translational value and better predict therapeutic efficacy.
For future directions, we look to bridge the gap between genetic risk and amyloid pathology. We developed a novel model by crossing APOE3/4 knock-in mice with ARTE10, an amyloid model. The resulting APOE3/4 x ARTE10 mice provide a powerful tool to study the interplay between APOE genotype and Aβ pathology and serve as a platform for preclinical testing of APOE-modulated therapies.
We also recognize the increasing development of human monoclonal antibody therapeutics for AD and other neurodegenerative diseases. This presents a unique opportunity to further refine AD models by integrating platform such as hTRFC and hCD98hc models, which enable blood-brain barrier (BBB) transcytosis.
Integrating BBB-penetrant systems into advanced AD models may enhance in vivo evaluation of biologics and accelerate the development of disease-modifying therapies.
November 17th, 2025, 1:00 p.m. - 5:00 p.m. | ALS and Motor Neuron Diseases: Animal Models
Amyloid Accumulation, Neuroinflammation and Loss of Motor Neurons Are the Hallmark of a SOD1 Rat Model of ALS | Session Number: PSTR212
In Collaboration with Psychogenics
Amyotrophic Lateral Sclerosis (ALS) is a progressive neurodegenerative disease that is characterized by muscle weakness, eventual paralysis, and death. There is no cure for ALS to date, and existing treatments focus on providing symptomatic relief and improving life quality. In collaboration with Taconic Biosciences, Inc, PsychoGenics characterized a new rodent model of SOD1 G93A-overexpressing (NTac:SD-Tg(SOD1G93A)L26H) rats. The results have indicated this model to be a valuable tool for researching ALS and developing potential therapies, as it replicates many key features of the disease, including motor neuron degeneration, muscle dysfunction, and increased neurofilament light chain (NfL) levels, a biomarker for neurodegeneration. In the current study, we used fixed frozen spinal cord sections derived from approximately 36-week-old male and female transgenic Sprague Dawley rats and wild-type littermates. Sections were labeled with a combination of antibodies to SOD1 amyloid [Pentameric formyl thiophene acetic acid (pFTAA) and superoxide dismutase (SOD1)], inflammatory markers [Glial Fibrillary Acidic Protein (GFAP) and Ionized calcium-binding adaptor molecule 1 (Iba1)], along with motor neuron markers such as choline acetyl transferase (ChAT) and neuronal nuclei (NeuN). Our data showed significant amyloid accumulation, accompanied by an increase in neuroinflammation, in the spinal cords of transgenic rats, confirming the disease pathology and associated neuroinflammation. A significant reduction in the number of motor neurons was also detected; however, the overall number of neurons in the spinal cord remained unaltered. Additional work is being done using specific new targets valuable in the field, such as lipid peroxidation and mitochondrial damage, as these have been shown to be implicated in ALS rodent models.
In summary, the SOD1 G93A rats show a significant amyloid accumulation, neuroinflammation and a loss of motor neurons in the spinal cord which leads to progressive muscle weakness and eventual paralysis. While the research is still ongoing, these initial findings indicate that this new rat model holds promise as a useful platform for screening potential novel therapeutics.
November 18th, 2025, 8:00 a.m. - 12:00 p.m. | APP/Abeta Pathway: Cellular and Animal Models
Behaviour and Biomarker Changes in ARTE10 mice reveal Translational Potential for Alzheimer’s Disease and Mood-Related Comorbidities | Session Number: PSTR266
In Collaboration with Transpharmation
Background: Alzheimer’s disease (AD) is characterized by progressive cognitive decline and hallmark neuropathological changes including amyloidβ (Aβ) plaque deposition. Patients often suffer from prodromal and co-morbid mood symptoms including anxiety and agitation which evade current therapies. The ARTE10 transgenic mouse model, which co-expresses human APP and PS1 mutations linked to familial AD, develops early and robust Aβ pathology. Previous studies have focused on cognitive changes and pathology in advanced stages of AD. Here we aimed to comprehensively characterize the ARTE10 model 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. Many behavioural domains were assessed with specific assays: 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 the levels of NfL and amyloid using the MesoScale Discovery platform and then correlated to behavioural results.
Results: Canopy test revealed increased anxiety-like behaviours in HM ARTE10’s via reduced distance in the open zone (p=0.0086), and decreased looking over the edge (p=0.0452) at 5 months. By 10 months, both endpoints progressed and remained significant (p<0.0001; p<0.0001). Nest building consistently demonstrated mood disturbances (5M: p=0.0006; 10M: p<0.0001), and running wheel evidenced consistent hyperactivity (5M: p=0.0233; 10M: p=0.0201) in ARTE10 animals. Spatial working memory deficits were only found at 10 months using Y maze (p=0.0039) and MWM (p=0.0429). Biomarker analysis revealed significantly increased Aβ42/40 ratio in the hippocampus (p=0.015) and cortex (p<0.0001) of 5 month ARTE10 mice. By 10 months amyloid load was further increased (p<0.0001). NfL was increased in the cortex (p=0.0016) and trending in CSF (p=0.06) at 5 months, these increased at 10M (cortex: p=0.0004, CSF: p=0.0037). Behaviour and biomarkers showed correlations between amyloid load and some behaviours.
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.
Our Presenters
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.
Sarah Sterlace, PhD
Scientific Portfolio Manager - Neuroscience
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.
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.
Maziyar Saberi, PhD
Vice President, Global Innovation
Maziyar Saberi, PhD, is a seasoned systems physiologist with a successful track record in target discovery and product development across therapeutics, nutraceuticals, and digital health products. He currently serves as Vice President of Global Innovations at Taconic Biosciences, where he leads R&D and acquisition strategies to drive the growth of Taconic's portfolio. Known for his ability to build innovative research platforms and advance preclinical programs, Mazi brings deep expertise in translational biology and scientific strategy. His career includes executive and senior roles at industry leaders, including January AI, Applied Molecular Transport, Second Genome Inc., and NGM Biopharmaceuticals. Mazi holds a PhD in Physiology and completed post-doctoral training in Neurophysiology at the University of Southern California, followed by a fellowship in Endocrinology and Metabolism at UC San Diego School of Medicine.
Lesley Tomlin
Vice President, Customer Solutions
Lesley Tomlin is a seasoned commercial executive with over 25 years of leadership experience in the life sciences and biotechnology sectors. She currently serves as Vice President of Global Sales, Marketing, and Customer Experience at Taconic Biosciences, where she leads global commercial strategy, brand development, and customer engagement. Known for her ability to build high-performing teams and drive strategic growth, Lesley brings deep expertise in go-to-market execution, digital marketing, and customer-centric operations. Her career spans senior roles at industry leaders including Roche Diagnostics, QIAGEN, and Life Technologies, with a consistent focus on advancing scientific innovation through strong commercial alignment. Lesley holds a Bachelor of Science in Biology from the University of Wisconsin–Madison.
Sarah Sterlace, PhD
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.
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.
Jennifer Pearson-Smith, PhD
Scientific Solutions Consultant
Dr. Jennifer Pearson-Smith has experience in metabolism, oxidative stress, and mouse colony management. At Taconic, she develops colony management solutions that meet the specific needs of the preclinical researchers she works with.
Amy Moring
Client Relationship Manager
Amy Moring joined Taconic in 2024 and as your local Client Relationship Manager for the Southwestern region, she is dedicated to supporting your pre-clinical studies by striving to offer the best solutions using in-vivo models. She is well-versed in Taconic’s portfolio of commercially available mouse and rat models to streamline your projects in a variety of therapeutic areas, as well as our custom model generation solutions and colony management services. Amy holds a Bachelors of Science in Microbiology from Cal Poly San Luis Obispo.
