What is Neurodegenerative Disease?
Neurodegenerative diseases are disorders caused by the deterioration of neurons in the brain. When there are changes of this kind in these cells they will function abnormally. This will eventually bring about their death. The neurodegenerative diseases AD, Parkinson’s disease (PD), Creutzfeldt-Jakob disease, and Multiple Sclerosis (MS) occur due to neuronal degeneration in the central nervous system. Current clinical treatments for these diseases have demonstrated inadequate results thus far.
Lifestyle modification presents a new possibility for neurodegenerative diseases. There is growing support in the scientific community for the belief that diseases like Alzheimer’s are preventable. They believe roles played by both inflammation and free radical activity in brain functional decline are common characteristics of neurodegenerative diseases. Even though there appear to be multiple factors that influence neurodegeneration, lifestyle choices made decades before symptoms appear may be critical determinants in the reduction of inflammation and the neuronal damage caused by free radicals. This is a key focus of preventive medicine in Cognitive health.
These Lifestyle choices can beneficially impact conditions like:
- Attention Deficit Hyperactive Disorder (ADHD)
- Headaches / Migraines
- Multiple Sclerosis (MS)
- Parkinson’s disease
- Post-Traumatic Stress Disorder (PTSD)
When inflammation is present in the brain, it appears to play a big part in neurodegenerative diseases. In fact, Inflammation is a common characteristic of all neurodegenerative conditions as it paves the way for free radical activation. This is a particularly troublesome phenomenon in the brain as free radicals typically attack neurons, the basic building block of the nervous system. Although similar to other cells in the human body in many ways, neurons differ from other cells as they are specialized to transmit information throughout the body. According to a 2006 article in The American Journal of Clinical Nutrition, findings indicate that the activation of microglia (tissue macrophages in the central nervous system) in response to injury, illness, aging, or other causes begins an inflammatory cascade of events.,. Initially, this cascade begins slowly. However, if allowed to accelerate it causes neuronal death, which activates more pro-inflammatory agents and creates a vicious cycle resulting in the brain-destroying enough neurons to cause the clinical signs of AD.
Maternal Inflammation and other Potential Links to the Development of Autism
A 2016 review published in 2016 provided insight into the growing epidemic of autism. In this review, a strong case is made that neuroinflammation (nervous tissue in the child’s brain) may be the causative factor that results in autism. There are a host of potential elements that could be causing neuroinflammation including maternal inflammation during fetal development, a diet poor in omega-3 fatty acids, and poor gut health due to inflammation in the infant during the infant’s first two years of life. At the most critical time in fetal neural network development, these dietary factors can disrupt growth and leave the fetus susceptible to developing autism.
Maternal infection has also been linked to autism. In 1964 the rubella outbreak was a worldwide health crisis which resulted in an almost 200-fold increase in autism in the infants born to mothers affected with the disease. Many theories explained that the viral infection caused heightened levels of inflammatory cytokines which crossed the placental barrier and caused elevated neuroinflammation in the developing fetal brain. However, you don’t need maternal infection to induce cytokine production in the fetal brain.
Oxidative Stress on the Mind
Another critical factor is the impact of oxidative stress on the brain. Clinical research has noted that patients with AD tend to have lower antioxidant levels than their healthy comparisons. According to researchers from a University of Kentucky in a 2007 Archives of Neurology study, autopsy findings on study patients with amnestic mild cognitive impairment demonstrate the presence of oxidative damage to lipids, proteins, DNA, and RNA in multiple brain regions in late-stage AD.
Studies indicate that Oxidative damage may be an early-stage indication of future symptoms of Alzheimer’s disease. The data also suggests that a combination of superior antioxidants and agents to improve defense mechanisms against oxidation will be required to neutralize this oxidative component and aid in stunting the pathogenesis of AD.
David Perlmutter, MD, FACN, a board-certified neurologist, a fellow of the American College of Nutrition, sums it up in two statements: “Body fat promotes inflammation. Body fat may store toxins. A fatter person even has a smaller hippocampus” and that “Neurodegenerative diseases represent the downstream effects of excessive of radical activity, supporting antioxidant approaches to brain protection and functional enhancement.”
Chess S. “Autism in children wit congenital rubella.” J Autism Childhood Schizophrenia 1:33-47 (1971).
Patterson PH. “Maternal infection and immune involvement in autism.” Trends in Mol Med 17:389-394 (2011).
Ashdown H et al. “The role of cytokines in mediating effects of prenatal infection on the fetus.” Mol Psychiarty 11:47-55 (2006).
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