Neuropathy "The Painful Enigma"

Approximately 5 million people in the United States have been diagnosed with Alzheimer’s disease (AD), one of the most common types of dementia, worldwide. A variety of factors can increase the risk of developing other types of dementia and AD, including poor diet and lifestyle habits. Research studies have also shown that treating the body as a whole may help prevent and, in several cases, even reverse cognitive decline. The goal is to start treatment immediately. In the following article, we will ultimately discuss how a functional medicine approach can help improve AD and other types of dementia.

Dementia and Alzheimer’s Disease Overview

Our brain is a complex organ made-up of about 100 billion neurons that are constantly communicating with each other. Also known as brain cells or nerve cells, neurons play a fundamental role in our cognitive function, including memory, thinking, and learning. Neurons are constantly repairing themselves, especially during sleep, but when brain cells or nerve cells can’t repair themselves, due to a variety of factors, it can ultimately affect cognition. Alzheimer’s disease is associated with a build-up of compounds, such as active microglial cells, tau proteins, and beta-amyloid plaques, among several others.

Because the body can’t break down these compounds, they can start to block the synapses where brain cells or nerve cells communicate with each other. This is believed to be one of the most common causes of AD and other types of dementia. Dr. Dale Bredesen, a renowned expert and neurologist, developed a breakthrough, alternative treatment option for dementia and AD that focuses on reducing glial cells, protein, and plaque build-up in the brain. According to Dr. Bredesen’s research studies, a build-up of these compounds can occur due to toxins, infections, inflammatory biomarkers, and genetics.

Alzheimer’s disease (AD) is one of the most common types of dementia among older adults. Research studies have demonstrated that pathological changes in the human brain, whether directly or indirectly, can ultimately cause loss of synaptic function, mitochondrial damage, microglial cell activation, and neuronal cell death. However, the pathogenesis of AD is not yet fully understood and there is currently no definitive treatment for the neurological disease. Research studies have demonstrated that the activation and priming of microglial cells may contribute to the pathogenesis of AD.

A proinflammatory status of the central nervous system (CNS) can also cause changes in the function of the microglial cells or microglia. Neuroinflammation is closely associated with the activation of microglia and astrocytes which are connected to a variety of neurological diseases by the synthesis and secretion of inflammatory mediators such as iNOS, ROS, and proinflammatory cytokines. According to research studies, microglial priming is also caused by the inflammation of the CNS.

Therefore, whether microglial priming is the result or the cause of neuroinflammation is still controversial. Microglial cell activation commonly causes an increase of Aβ and tau proteins as well as a decrease of neurotrophic factors, ultimately leading to the loss of healthy brain cells or neurons and the development of neuritic plaques and neurofibrillary tangles which are closely associated with AD. With the progression of Alzheimer’s disease, changes from neuronal dysfunctions which may have no obvious symptoms to memory loss and cognitive impairment may become more noticeable.