Safely and Effectively Reverse AD/PD, Precision Medicine MEE N5195-II, Vision 3.0 by MEEOM® 
Oct. 20,  06:32 am JST 
 
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AD
Decreased proteins, not amyloid plaques, are tied to Alzheimer's disease. Led by Alberto Espay, MD, and Andrea Sturchio, MD, in collaboration with the Karolinska Institute in Sweden, published the research on Oct. 4 in the Journal of Alzheimer's Disease.
 
Overview
We conducted a retrospective longitudinal study among mutation carriers participating in the Dominantly Inherited Alzheimer Network (DIAN) cohort study. The DIAN study longitudinally evaluates families with dominantly inherited AD and non-carrier relatives of the probands. Details about the DIAN study design can be found in previous publications [1, 2]. We included all mutation carriers with at least two follow-up visits including baseline, without applying any other inclusion/exclusion criteria. All analyses were conducted in two cohorts: 1) amyloid PET-positive cohort, the most critical as these are individuals considered at greater risk for developing dementia; and 2) overall cohort, which included both amyloid PET-positive and amyloid PET-negative subjects.
 
Clinical assessment
Each assessment comprised a detailed medical history, neurological, and neuropsychological examination. Cognitive function was primarily quantified using the Clinical Dementia Rating scale (CDR = 0, indicates normal cognition; 0.5, very mild dementia; 1, mild dementia; 2, moderate dementia; and 3, severe dementia) [3]. Our primary endpoint was CDR progression, defined as any increase in CDR over the follow-up period. Secondary endpoints were progression to CDR ≥0.5 confirmed in two consecutive visits as per DIAN guidelines to minimize misclassification, progression to CDR ≥1, Mini-Mental State Examination (MMSE) score ≤24 at last visit (higher means better cognition) [4], and a CDR sum of boxes (CDR-SB) score ≥4.5 at last visit (lower means better cognition) [5]. CDR-SB = 4.5 corresponds to mild dementia [5].
 
Sample size calculation
In a previous cross-sectional study of PiB-PET-positive individuals, we found that higher CSF Aβ42 levels were associated with greater odds of normal cognition than AD (adjusted odds ratio [OR], 6.26; p < 0.001) or mild cognitive impairment (OR, 1.42; p = 0.006) [6]. Using these results, a sample size of 105 PiB-PET-positive mutation carriers was calculated to yield >80% power to detect a significant association (OR >1.85) between soluble Aβ42 levels (assuming continuous normal distribution) and the primary (CDR progression) and secondary endpoints (progression to CDR ≥0.5, progression to CDR ≥1, MMSE ≤24, CDR-SB ≥4.5) using multiple logistic regression with a two-sided Wald test after adjusting for other independent variables with a coefficient of determination (R2) of 15% and baseline probability of outcome of 50%.  Sample size estimation and simulations were carried out using PASS 2021 (Power Analysis and Sample Size Software [2021]. NCSS, LLC. Kaysville, UT, USA, ncss.com/software/pass).
 
PD
In Parkinson's disease, a normal soluble protein in the brain called alpha-synuclein can harden into a deposit called a Lewy body. The researchers hypothesize that Parkinson's is not caused by Lewy bodies aggregating in the brain, but rather by a decrease in levels of normal, soluble alpha-synuclein.
 
"We're advocating that what may be more meaningful across all degenerative diseases is the loss of normal proteins rather than the measurable fraction of abnormal proteins," Espay said. "The net effect is a loss not a gain of proteins as the brain continues to shrink as these diseases progress."
 
Espay said he envisions a future with two approaches to treating neurodegenerative diseases: rescue medicine and precision medicine.
 
MEEOM® Precision Medicine has been effectively reversing AD/PD members since 2020. Protecting your loved ones' wholehearted smiles with MEE N5195-II, Vision 3.0, which is safe and more effective.
 
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The MEEOM® approach is inclusive, effective and tailored to the needs of each individual. We do a rigorous assessment with each client at the beginning of treatment, to help us understand the person and the specific problems they want to address through treatment.
 
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SUPPLEMENTARY MATERIAL
REFERENCES
[1] Bateman RJ , et al,  (2012) Clinical and biomarker changes in dominantly inherited Alzheimer’s disease, N Engl J Med 367, 795–804. Erratum in: N Engl J Med 367, 780.
[2] Morris JC , et al, Buckles VD (2012) Developing an international network for Alzheimer research: The Dominantly Inherited Alzheimer Network, Clin Investig (Lond) 2, 975–984.
[3] Morris JC (1993) The Clinical Dementia Rating (CDR): Current version and scoring rules, Neurology 43, 2412–2414.
[4] Creavin ST , et al, Cullum S (2016) Mini-Mental State Examination (MMSE) for the detection of dementia in clinically unevaluated people aged 65 and over in community and primary care populations, Cochrane Database Syst Rev 2016, CD011145.
[5] O’Bryant SE , et al; Texas Alzheimer’s Research Consortium (2008) Staging dementia using Clinical Dementia Rating Scale Sum of Boxes scores: A Texas Alzheimer’s research consortium study, Arch Neurol 65, 1091–1095.
[6] Sturchio A , et al, (2021) High cerebrospinal amyloid-β 42 is associated with normal cognition in individuals with brain amyloidosis, EClinicalMedicine 38, 100988.