Parkinson’s Disease

Parkinson’s Disease

According to the Parkinson’s Disease Foundation, “Parkinson’s disease is a chronic and progressive movement disorder.” While the exact cause is unknown, more than one million people are suffering from Parkinson’s Disease (PD). The pathology of PD is linked to damaged neurons that produce dopamine in a specific region in the brain called the substantia nigra. A loss of dopaminergic neurons often results in symptoms including tremors, bradykinesia, rigidity, and instability. Other symptoms associated with PD include sleep disturbances, reduction in a sense of smell, mood disorders, fatigue, depression, constipation, and bladder complications.

NAD+ Within The Cell

Nicotinamide adenine dinucleotide (NAD+) is a coenzyme found within every cell to help drive enzymatic reactions forward, especially reactions that produce cellular energy. In addition, NAD+ also influences gene expression relating to DNA repair, cell death, and certain anti-inflammatory processes. Learn how IV nutrition therapy is an effective way to increase NAD+ levels.

Mitochondrial Function and Parkinson’s

Mitochondria are the powerhouses of our cells. Without our mitochondria, we would not be able to perform everyday activities. In addition to creating energy, mitochondria also play a role in calcium regulation and, when dysfunctioning, can initiate programmed cell death. Thus, mitochondrial dysfunction has become one of the proposed theories driving PD.

Damage to the mitochondria, along with low levels of NAD+, can significantly alter the cell’s ability to produce energy and maintain proper function. The natural process of aging also contributes to the decline of mitochondrial function by decreasing expression of genes associated with energy metabolism (which is associated with the pathology of PD).  Neurons are especially susceptible to energy fluctuations due to mitochondrial dysfunction. Damaged neurons can lead to the pathogenesis of several neurodegenerative diseases, including PD.

Sirtuins

NAD+ has the ability to regulate a class of proteins known as sirtuins, or silencing information regulators. Sirtuins play a vital role in regulating anti-inflammatory processes throughout the body and the brain. Many studies have linked the neuroprotective effects of sirtuins and its implications to Alzheimer’sParkinson’sdementiamultiple sclerosis, and amyotrophic lateral sclerosis (ALS).

It has also been observed that NAD+ levels fluctuate in Parkinson’s cells, and thus alter the expression of sirtuins. Increased expression of sirtuins due to increased production of NAD+ has been shown to promote neurogenesis, or the growth and development of new neurons.

PARPs

Poly (ADP-ribose) polymerases (PARP) are another class of enzymes that play a key role in DNA repair. While these enzymes are crucial for cell health, they place a heavy tax on mitochondria by depleting levels of NAD+. In the case of excessive oxidative stress and DNA damage, programmed cell death is initiated by lack of NAD+.

Conventional Treatment for Parkinson’s

Treatment for PD often includes two types of prescription medications, Levodopa and dopamine agonists. Levodopa, and other similar drugs, are converted to dopamine within the brain. This is considered the gold standard of PD treatment because of its effectiveness in reducing symptoms. On the other hand, dopamine agonists bind to dopamine receptor sites, allowing the brain to ‘think’ it has the dopamine it needs. Other types of drugs are often prescribed to help Levodopa perform more efficiently within the brain.

Prescription drugs only help reduce the symptoms of PD. There is no widely accepted preventative measure that treats the underlying pathology for PD to date. Every year 60,000 new people are diagnosed with PD and $25 billion is spent to treat PD annually. The pressure for effective preventative measures and curative treatments for PD is rising with each new diagnosis.

Recent research on NAD+ therapy has shown promising therapeutic benefits to many neurodegenerative diseases, including PD.

Toxic Exposure in Parkinson’s

A common pesticide rotenone has been linked to the pathology of Parkinson’s. Rotenone is known to inhibit a key enzyme involved in energy metabolism within the mitochondria, as well as the formation of a-synuclein. A combination of a dysfunctional mitochondria and accumulation of a-synuclein are two key factors in the formation of Lewy bodies, or the aggregation of damaged proteins within neuronal cells. Lewy bodies are a known causative factor for PD.

Parkinson’s disease is due to a spectrum of pathologies and causative factors. The NAD Treatment Center is investigating Parkinson’s disease through patient responses in which NAD+ therapy is most effective.