Alzheimer's disease is a neuroinflammatory, neurodegenerative condition characterized by progressive cognitive decline, including short-term memory loss and executive function deterioration. 6 million people have been diagnosed with Alzheimer's in the US.
Historically, diagnosing Alzheimer's relied on post-mortem confirmation of extra neuronal amyloid beta (Aβ) plaques. Recent advancements in brain imaging can now detect Aβ plaques in individuals with dementia.
More recently, approved tests measure Aβ levels in the brain or blood, aiding Alzheimer's diagnosis in clinical trials and guiding Aβ-targeted therapy for different dementia types. We appreciate Aβ research's contributions to targeted therapies and believe further progress is achievable.
A Different Approach
BioVie's perspective centers on inflammation as the core driver behind Alzheimer's disease development and progression. BioVie takes a distinctive approach by focusing on an innovative compound, bezisterim (NE3107), currently undergoing research in individuals diagnosed with Alzheimer's disease.
At BioVie, we believe that selectively modulating inflammation and enhancing energy transfer (insulin sensitivity) in the brain could potentially enhance memory and cognitive function while safeguarding against neurodegeneration. If our research proves successful, bezisterim may offer future advantages to the vast number of Alzheimer's patients, as well as their caregivers, families, and healthcare professionals.
Pathology & Physiology
Alzheimer’s disease (AD) is one form of dementia, and it is believed to be a neuroinflammatory and, 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 may actually begin decades before noticeable symptoms are observed.
Because there a numerous potential forms of dementia, the formal diagnosis of Alzheimer’s disease as one particular type of dementia 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 sometimes be found in people without apparent AD symptoms, and AD-like dementia can also occur without Aβ plaques. These observations have led to healthy scientific debate about the role of Aβ within the overall context of AD pathology. Hence, the question of what initiates AD has not yet been fully settled.
Nonetheless, there is a large and increasing scientific literature supporting the concept that inflammation, in concert with insulin resistance, metabolic dysregulation, and stress may play a pivotal role in the onset and progression of AD. An increasing portion of researchers are referring to Alzheimer’s as “Type 3” diabetes. This metabolic inflammation “theory” of AD recognizes the contribution of diverse elements to the disease process, with inflammation having a central role.
Data pointing to the confluence of inflammation and insulin resistance in dementia is fueling an interest in developing therapies that target metabolic dysregulation in AD.
