Alzheimer’s disease

Pathology and Physiology Overview

Alzheimer’s disease (AD) is a neuroinflammatory, neurodegenerative condition, characterized by progressive deterioration of short-term memory and problem-solving ability. Disease onset is generally observed after 60 years of age, although there is evidence that disease processes actually begin decades before noticeable symptoms are observed.

Formal diagnosis of Alzheimer’s disease has historically been dependent on the presence of deposits (plaques) in the brain made of amyloid beta (Aβ), a protein involved in neural growth. However, Aβ plaques can also be found in people without apparent AD symptoms, and AD-like dementia can occur without Aβ plaques. These observations have cast doubt about the role of Aβ as the sole central mediator of AD pathology. There is no scientific consensus regarding specifics of what initiates AD. However, there is an immense amount of information indicating that inflammation in concert with insulin resistance, metabolic dysregulation, and stress has a pivotal role in AD. This metabolic inflammation “theory” of AD recognizes the contribution of diverse elements to the disease process, with inflammation having a central role.

This confluence of inflammation and insulin resistance is fueling the growing interest in developing therapies that target metabolic dysregulation in AD.

Targeting inflammation may hold the key to unlocking new advancements in Alzheimer’s disease therapies

NE3107 has shown promise in Alzheimer's Disease:
  • Growing body of evidence shows the promise of reducing neuroinflammation in Alzheimer’s
  • Additional key benefit of NE3107 is the potential to reduce insulin resistance
  • Potential for excellent safety profile based on pre-clinical and clinical trials
  • Pivotal Phase III study has been initiated

Mechanism of Action

NE3107’s mechanism acts on the fundamental inflammatory signaling pathways that are the root cause of Alzheimer’s and other neurodegenerative diseases. NE3107 selectively inhibits the inflammatory ERK signaling pathway that reduces neuroinflammation by inhibiting inflammation-driven insulin resistance and major pathological inflammatory cascades.

Because both inflammation and insulin signaling contribute to Alzheimer’s disease dementia, BioVie believes that clinical trials may show that the drug slows the progression of Alzheimer’s disease as well as improving cognition and function as related to activities of daily living.
Forward Looking Statements
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