Diet plays a large role in inflammation, oxidative stress and cognition; however, every person's body type, resting metabolic rate, BMI, and inflammation levels vary. Through performing physiological and comprehensive cellular testing through bio-impedance, allows this study to create personalized diet plans for each subject's body type. Cellular repair therapy has also been known to improve cellular health and inflammation. Through decreasing inflammation and improving oxidative stress, cognition in those with MCI and AD could improve.
Even though AD has been associated with specific hallmarks, multiple etiologies have been suggested to be prominent in the pathogenesis of the disease. Chronic inflammation, metabolic dysfunction, oxidative stress and mitochondrial damage have all been linked to the incidence and progression of neurodegeneration, negatively impacting overall prognosis of AD. Currently, only a handful of FDA approved Alzheimer's medications are on the market; yet, these medications are known to only treat symptoms associated with AD, not the underlying causes. There are currently no medications FDA approved for MCI and predicting who will progress onto AD is unknown. Unfortunately, in the last decade alone, several clinical trials in MCI and AD, have been terminated prior to study conclusion, due to lack of efficacy and/or poor study design. Even if an experimental drug is shown to be promising in early stages of testing, it could take up to another 10-15 years before it is FDA approved and made commercially available. Therefore, the need to find a therapy that could possibly prevent people with MCI from developing AD is imperative. Through studying different etiologies, providing a specialized diet based on each subject's individual physiological results and improving mitochondria through cell repair therapy, not only can be quickly implemented into the life of a person with cognitive impairment, but could possibly decrease the prevalence and slow disease progression of AD. Thus, the fundamental research of this study is to determine if such etiologies are measurable in patients with MCI and AD through body composition and cellular health testing that could lead to proper and novel treatments to combat the diseases. This study was conducted in hopes of determining that chronic inflammation and other risk factors for MCI and AD such as oxidative stress and metabolic dysfunction, can be ameliorated, improve cognitive function, and therefore prevent disease progression through effective, non-drug therapies.
Study Type
INTERVENTIONAL
Allocation
NA
Purpose
TREATMENT
Masking
NONE
Enrollment
5
Specialized anti-inflammatory diet plan based on subject's physiological results
the objective of this type of technology is to support the body's own processes to repair protein structures and maintain the health of the DNA, both of which have been damaged by internal and external factors.
Perseverance Research Center, LLC
Scottsdale, Arizona, United States
Change in inflammation as measured through bioimpedance analysis from baseline to week 12
Mito-Food plan with cellular repair therapy will decrease inflammation in MCI and AD patients
Time frame: 3 months
Change in Mini Mental State Exam (MMSE) from Baseline to Week 12
Measuring cognition over the course of treatment as measured by the MMSE
Time frame: 3 months
Change in Montreal Cognitive Assessment (MoCA) from Baseline to Week 12
Measuring cognition over the course of treatment as measured by the MoCA
Time frame: 3 months
Change in Quality of Life in Alzheimer's Disease (QOL-AD) from Baseline to Week 12
Determining if scores on Quality of Life in AD improves over course of therapy
Time frame: 3 months
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