Designed by scientists
Since over 50 million people worldwide are currently diagnosed with dementia, and this number doubles every 20 years (Prince, 2015), early diagnosis of dementia is one of the key requirments for maintaning healthy life and healthy aging. Although the current diagnostic protocol is based on NINCDS-ADRDA Alzheimer’s criteria (McKhann, 1984), it is known that changes associated with Alzheimer’s begin 20 or more years before symptoms appear (Villemagne, 2013; Jack, 2009; Bateman, 2012). Thus one of the main reasons for shockingly high rate of failure of clinical trials which test new drugs for Alzheimer’s disease is the fact that the disease is diagnosed too late (Cummings, 2019).
Started from facts known for several decades that some molecules like beta-amyloid and tau are highly involved in pathogenesis of disease, many laboratories were working hard to establish a method which will:
- allow to obtain a sample of cells which will precisely mirror the processes occurring in the brain (since brain biopsy is not a routine method and blood tests are useless since the brain is hidden behind the blood brain barrier) and
- correlate observed levels of proteins with the stage of pathological process.
In addition, it became clear that only by precise/personalized medical approach based on the tailored instructions for the specific needs of the individual brain, we can slow down, stop and revert the pathological process (Keine, 2018)
Gathered in an international consortium which involved several laboratories (M.Song Republic of Korea; J. Wang, China; J. Isaković, UAE; D. Mitrečić, Croatia, and many others), we applied the latest advances in stem cell technology to develop a simple method to transform cells residing in the root of the hair into neurons. Since then, ourselves and other medical practitioners have published that brain cells obtained in this way precisely mirror pathological process occurring within donor body, the first requirement of obtaining a simple and reliable source of cells was in this way fulfilled. Based on meticulous follow up of more than 2000 individuals in seven countries, we developed an original approach in which an absolute concentration of molecules – which have been already reported as possible markers of Alzheimer`s dementia – can now be replaced by a relative scale in which measurements obtained in two different time points give us critical information about the rate of accumulation of the proteins of interest. By analysing familiar cases of Alzheimer`s dementia, in which we measured more than 70 proteins linked to disease, we were able to obtain curves which now represent a firm basis for numerical estimation of the individual current risk of entering into a symptomatic phase of the disease. Moreover, this enables us to recognize patterns of fast or slow progressing disease, which also correlates with the response to specific types of available therapies.
Most importantly, this approach allows us to quantify a set of critical parameters needed for a fine-tuned strategy to prevent, stop and revert dementia, all tailored and designed for the specific needs of the individual brain.
In other words, Check My Brain gives you three types of information:
- estimates your specific risk of developing disease,
- discovers the disease on time, much before other tests can discover it and
- recommends how to slow down, stop or revert pathological process within your brain.
In conclusion – Check My Brain is the test designed by experts and based on the knowledge published in several hundreds peer-reviewed publications. This very concept represents a current leading edge in the early diagnostic of Alzheimer`s disease and as such is protected by patent application. The whole concept is gathered and owned by Omnion Research International ltd, an international medical company registered in Zagreb, Croatia, European Union.
Check My Brain is fully certified by the regulatory agency as a diagnostic medical product.
References
Alajbeg I, Alić I, Andabak-Rogulj A, Brailo V, Mitrečić D. Human- and mouse-derived neurons can be simultaneously obtained by co-cultures of human oral mucosal stem cells and mouse neural stem cells. Oral Dis. 2018 Mar;24(1-2):5-10.
Alić I, Kosi N, Kapuralin K, Gorup D, Gajović S, Pochet R, Mitrečić D.Neural stem cells from mouse strain Thy1 YFP-16 are a valuable tool to monitor and evaluate neuronal differentiation and morphology. Neurosci Lett. 2016 Nov 10;634:32-41.
Bateman RJ, Xiong C, Benzinger TL, Fagan AM, Goate A, Fox NC, et al. Clinical and biomarker changes in dominantly inherited Alzheimer’s disease. N Engl J Med 2012;367(9):795-804.
Cummings J, Lee G, Ritter A, Sabbagh M, Zhong K. Alzheimer’s disease drug development pipeline: Alzheimers Dement (N Y). 2019 Jul 9;5:272-293.
Essayan-Perez S, Zhou B, Nabet AM, Wernig M, Huang YA. Modeling Alzheimer’s disease with human iPS cells: advancements, lessons, and applications. Neurobiol Dis. 2019 Oct;130:104503.
Isakovic J, Dobbs-Dixon I, Chaudhury D, Mitrecic D. Modeling of inhomogeneous electromagnetic fields in the nervous system: a novel paradigm in understanding cell interactions, disease etiology and therapy. Sci Rep. 2018 Aug 27;8(1):12909.
Isaković J, Gorup D, Mitrečić D. Molecular mechanisms of microglia- and astrocyte-driven neurorestoration triggered by application of electromagnetic fields. Croat Med J. 2019 Apr 30;60(2):127-140.
Jack CR, Lowe VJ, Weigand SD, Wiste HJ, Senjem ML, Knopman DS, et al. Serial PiB and MRI in normal, mild cognitive impairment and Alzheimer’s disease: Implications for sequence of pathological events in Alzheimer’s disease. Brain 2009;132:1355-65.
Keine D, Walker JQ, Kennedy BK, Sabbagh MN. Development, Application, and Results from a Precision-medicine Platform that Personalizes Multi-modal Treatment Plans for Mild Alzheimer’s Disease and At-risk Individuals. Curr Aging Sci. 2018;11(3):173-181
Mitrečić, D. Current advances in intravascular administration of stem cells for neurological diseases: A new dose of rejuvenation injected. Rejuvenation research: 2011; 14(5):553-5.
Ochalek A, Mihalik B, Avci HX, Chandrasekaran A, Téglási A, Bock I, Giudice ML, Táncos Z, Molnár K, László L, Nielsen J, Holst B, Freude K, Hyttel P, Kobolák J, Dinnyés A. Neurons derived from sporadic Alzheimer’s disease iPSCs reveal elevated TAU hyperphosphorylation, increased amyloid levels, and GSK3B activation. Alzheimers Res Ther. 2017 Dec 1;9(1):90.
Villemagne VL, Burnham S, Bourgeat P, Brown B, Ellis KA, Salvado O, et al. Amyloid ß deposition, neurodegeneration, and cognitive decline in sporadic Alzheimer’s disease: A prospective cohort study. Lancet Neurol 2013;12(4):357-67.
Wei S, Gao L, Jiang Y, Shang S, Chen C, Dang L, Zhao B, Zhang J, Wang J, Huo K, Wang J, Zhang R, Qu Q. Apolipoprotein E ε4 Allele is Associated With Plasma Amyloid Beta and Amyloid Beta Transporter Levels: A Cross-sectional Study in a Rural Area of Xi’an, China. Am J Geriatr Psychiatry. 2019 Jun 28.