WE STRIVE TO PREVENT AND CURE DEMENTIA

For decades, Eisai has led the way in dementia research and development. Now we’re broadening our scope, taking a multi-dimensional, targeted path to our ultimate goal: prevention and a cure. Here’s a quick look at what we’re working on right now.

HERE’S OUR PRECISION APPROACH TO ACCELERATING NEUROLOGY ADVANCES

Building on 30 years of researching and understanding dementia, we’re striving to prevent and cure dementia and AD. Our precision approach to drug discovery research includes:

Human biology: We're leveraging recent genetics research to explore using immunology to regulate processes and mechanisms in certain neurologic conditions.
Translational sciences: By focusing on translational biomarker research early in the discovery process, our scientists can quickly identify which patients might respond to certain therapies.
Collaboration-based research: We’re sharing our own research and working in partnerships with other experts to accelerate drug discovery and development.
Diagnostics: We’re collaborating with other experts to develop and commercialize simple, cost-effective tools that can easily and accurately help health care professionals screen and diagnose AD.

A BLOOD TEST FOR ALZHEIMER’S?

We’re collaborating with Sysmex on a potential blood-based test for predicting amyloid pathology. This automated immune-assay system under investigation could also be utilized as a simpler and more cost-effective method to identify participants for clinical trials exploring a variety of AD therapies now in development.

Critical insights from leading experts about the science behind the Aβ pathway in Alzheimer’s disease

Reflecting over three decades of progress in molecular medicine, amyloid-β (Aβ) remains the hallmark of Alzheimer’s disease (AD) pathology and is the leading target for developing potential disease-modifying therapies. Presented at the 15th International Conference on Alzheimer’s & Parkinson’s Diseases (AD/PDTM 2021), the presentations summarize the latest updates and supporting evidence of the role of Aβ in AD by synthesizing the existing and new translational & cross-disciplinary data-driven studies.

“Extensive evidence indicates that Aβ accumulation in the brain is one of the earliest pathophysiological changes in the Alzheimer’s disease continuum, and that early targeting of the pathway may provide a promising therapeutic approach to prevent or slow down the clinical biological progression of the disease.”

Dr. Harald Hampel
Chief Medical Officer
Neurology Business Group

Negative clinical trial outcomes over two decades in anti-Aβ drug development do not negate the central role of Aβ as one of the earliest pathophysiological mechanisms in the AD clinical biological continuum. Here, Dr. Jeffrey Cummings provides a high-level overview of the cross disciplinary literature based on genetic, epigenetic and biological data that support the pathophysiological role of the Aβ pathway in the biological continuum of AD.
Historical and evolving evidence support a hypothetical model of AD pathophysiology characterized by accumulation of Aβ species in the brain decades before clinical manifestations and prior to other pathophysiological hallmarks. Dr. John Hardy provides a state-of-the-art overview of the biological and genetic evidence supporting the critical role of Aβ in AD.
The Aβ pathway encompasses several aggregation species of Aβ from monomers, oligomers, protofibrils, fibrils, to plaque. Here, Dr. Colin Masters describes how various aggregation species relate to Aβ bioactivity in the AD brain and how loss of Aβ homeostasis may result in synaptic failure, which underlies cognitive deficits spanning learning and memory.
Pathophysiological changes of Aβ homeostasis can be assessed and quantified in vivo using molecular neuroimaging (i.e., PET) or biofluids such as cerebrospinal fluid and blood. Here, Dr. Philip Scheltens provides a state-of-the-art overview of the different biomarkers charting the Aβ pathway.

Alzheimer’s disease: global impact, pathophysiology, and the evolving clinical care

Alzheimer’s disease is a growing global health challenge and has an enormous impact on patients and family members, healthcare systems and society at large. In the three videos below, Dr. Harald Hampel, Vice President and Chief Medical Officer of the Neurology Business Group, and a global expert in Alzheimer’s Disease discusses the global impact of dementia due to Alzheimer’s and other neurodegenerative diseases. In addition, he presents existing multi-disciplinary evidence that supports the role of the amyloid-β pathway in Alzheimer’s disease pathophysiology and therapy development. Finally, he provides future perspectives on Alzheimer’s disease research and clinical care.

The prevalence of dementia due to Alzheimer’s disease and other neurodegenerative diseases is rising rapidly worldwide with increases in population aging and growth. Here, Dr. Hampel summarizes the current and projected epidemiology of dementia, as well as the associated societal and economic cost both at the global level and in Japan as a country-specific example.
Impairment of amyloid-β (Aβ) metabolism and consequent accumulation of Aβ aggregation species in the brain is an early and central event in Alzheimer’s disease pathophysiology. Here, Dr. Hampel discusses biological and clinical evidence linking alteration of the Aβ cycle to Alzheimer’s disease progression across the preclinical, prodromal, and dementia stages.
In this video, Dr. Hampel discusses the road ahead in Alzheimer’s science and clinical diagnosis and management of the disease. Highlighting the AT(N) framework, he presents the steps toward precision medicine and delivers an overview of recent advances in biomarker development — in particular, blood and digital biomarkers for globally accessible and sustainable solutions to Alzheimer’s disease healthcare.

Learn from leading AD experts about the AT(N) system and how it may shape clinical practice and therapy development

Discover the AT(N) system – a biomarker-based classification system that classifies individuals using core AD pathophysiological features: amyloid-β(A), tau (T) and neurodegeneration (N). Presented at the 2020 Alzheimer’s Association International Conference (AAIC), the three presentations provide a state-of-the-art overview on the validation and qualification of the AT(N) system and its evolution to ATX(N) for AD clinical practice and therapy development.

“The AT(N) system offers a framework to define Alzheimer’s disease in a continuum using biologically rooted measurements. It circumvents the limitations of the traditional, clinical phenotype-based approach, and has the potential to facilitate therapeutic interventions at the early stages of the disease.”

Harald Hampel
Chief Medical Officer
Neurology Business Group

Dr. Jeffrey Cummings provides an overview of the conceptual framework and significance of the AT(N) system.
Dr. Clifford Jack describes the history of the AT(N) system and discusses its potential contexts-of-use in clinical trials and clinical care.
Dr. Kaj Blennow provides a state-of-the-art and perspectives on the development of CSF and blood biomarkers of the AT(N) system.