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.