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Alzheimer's

Alzheimer's disease is characterized by the premature death of neurons, leading to a neurodegenerative process that manifests itself at the cerebral level by the presence of neuritic plaques in the form of β-amyloid deposits and neurofibrillary tangles formed by hyperphosphorylation of the Tau protein, reflecting alterations in the cytoarchitecture of neurons. At the clinical level, Alzheimer's disease manifests progressively and irreversibly with memory impairment, behavioral alterations and psychomotor decline.

Alzheimer's disease is a priority health problem in developed countries, with great socio-familial, socioeconomic and socio-health impact. Alzheimer's disease is the leading cause of dementia (>50%), followed by vascular dementia and mixed dementia, with a prevalence of 1% at age 60 years and more than 35% in people over 80 years. The cost of dementia in European countries fluctuates between €10,000 and €25,000 per patient per year, depending on the degree of deterioration, stage of the disease, and care model.

Alzheimer's is a complex and multifactorial disease caused by:

  1. multiple defects in the human genome

  2. epigenetic aberrations that alter the normal expression of genes

  3. cerebrovascular alterations responsible for lack of cerebral oxygenation

  4. neuroinflammatory and cytotoxic reactions

  5. failure of neurotrophic mechanisms to maintain neuronal survival

  6. oxidative phenomena that alter the metabolism of the brain

  7. multitude of environmental processes that cause brain damage (microtrauma, toxic substances, inadequate drugs, poor nutrition).

Alzheimer's disease, in particular, and dementia, in general, have an important genetic and familial component, the risk of which increases with pernicious environmental factors and/or concomitant diseases (stroke, migraine, cardiovascular disorders, arterial hypertension, hypercholesterolemia and dyslipidemia, diabetes, hypothyroidism, anemia and deficiency syndromes associated with folic acid and vitamin B12 deficiency).

 

There are more than 600 genes distributed throughout the human genome whose mutational defects or alterations in gene expression contribute to the neurodegeneration process associated with Alzheimer's disease. Mendelian mutations in some of these genes cause familial forms of early Alzheimer's disease; and other genetic variants represent susceptibility elements that increase the risk of dementia in families where these genetic defects accumulate.

 

A fundamental characteristic of Alzheimer's is that this disease, although it manifests itself in adulthood and senescence, is actually undermining the brain of the population at risk since the brain stops maturing around the age of 30 and takes about 3 decades to show symptoms. By the time memory failures appear, the brain damage is already so significant that conventional pharmacological treatments are ineffective and fail to improve symptoms or interrupt the destructive process of the disease.

Alzheimer's Prevention Plan

There are currently 4 drugs with low efficacy for the treatment of Alzheimer's disease, developed before 2005. During the last 15 years no new drug has been approved by international regulatory agencies to treat this disease. Convinced by the evidence, the international scientific community is becoming convinced that the only way to defeat Alzheimer's is to intercept the disease years before it manifests its first symptoms, for which it is urgent to implement preventive plans to protect the population at risk.

 

The International Center for Neurosciences and Genomic Medicine, directed by Dr. Ramón Cacabelos, Professor of Genomic Medicine and internationally recognized scientist, is a world reference center in neurodegenerative diseases, with more than 1,500 scientific contributions and a vaccine (EB-101) approved by the United States Patent Office for the prevention of Alzheimer's disease.

 

The medical and scientific team of EuroEspes has developed in recent years a Selective Program for the prevention of dementia in the population at risk.

 

Prior to this medical program, it is possible to request genetic tests, which allow us to obtain the necessary information to evaluate the risk of developing Alzheimer's disease.

Modalities

This program comprises 3 modalities:

  1. Prevention Plan for first and second generation relatives with family history of dementia
  2. Prevention plan for people with cardiovascular and/or cerebrovascular diseases that represent risk factors for dementia.
  3. Dementia Prevention Plan in the general population.

The integrated medical intervention model:

  1. Medical examination
  2. Analytical testing (biochemistry, hematology, metabolism, neurochemistry, epigenetic biomarkers)
  3. Neuropsychological testing (cognitive and intellectual performance, emotional and behavioral status, psychomotor function)
  4. Static and functional neuroimaging with state-of-the-art neurotechnology
  5. Predictive and pathogenic genomic analysis
  6. Personalized preventive and/or therapeutic intervention program based on individual pharmacogenomics.

The program has been designed with international projection, oriented to the European, Asian and Latin American population.

On the occasion of World Alzheimer's Day and the launching of the Alzheimer's Prevention Plan, you can review the most important interventions and interviews of Dr. Cacabelos in various media:

  • Cacabelos R. Population-level pharmacogenomics for precision drug development in dementia. Expert Review of Precision Medicine and Drug Development, 2018;3:3; 163-188. DOI: 10.1080/23808993.2018.1468218.
  • Cacabelos R, Cacabelos N, Carril JC. The role of pharmacogenomics in adverse drug reactions. Expert Rev Clin Pharmacol, 2019;12(5):407-442. DOI: 10.1080/17512433.2019.1597706. Epub 2019 Apr 24.
  • Cacabelos R. Pharmacogenomics of Cognitive Dysfunction and Neuropsychiatric Disorders in Dementia. Int J Mol Sci, 2020;21(9):E3059. DOI: 10.3390/ijms2109303059.
  • Cacabelos R. Pharmacogenomic of drugs to treat brain disorders. Expert Review of Precision Medicine and Drug Development 2020. DOI: 0.1080/23808992.2020.1738217.
  • Cacabelos R. Pharmacogenetic considerations when prescribing cholinesterase inhibitors for the treatment of Alzheimer's disease. Expert Opinion on Drug Metabolism & Txicology, 2020;16(8):673-701. DOI: 10.1080/17425255.2020.1779700.

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