Alzheimer's Disease

Alzheimer's is characterised by premature death of neurons, resulting in a neurodegenerative process that manifests itself at the brain level by the presence of neurotic plaques in the form of β-amyloid deposits and neurofibrillary balls formed by hyperphosphorylation of the Tau protein, which reflects alterations in the cytoarchitecture of neurons. At the clinical level, Alzheimer's develops progressively and irreversibly with memory disorder, behavioural disturbances, 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 is the leading cause of dementia (>50%), followed by vascular dementia and mixed dementia, with prevalence of 1% at age 60 and more than 35% in people over the age of 80. The cost of dementia in European countries fluctuates between 10,000 and 25,000 euros per patient per year, depending on the degree of deterioration, stage of the disease, and care model.

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

  1. multiple defects in the human genome

  2. epigenetic aberrations that alter the normal expression of genes

  3. strokes responsible for lack of brain oxygenation

  4. neuro-inflammatory and cytotoxic reactions

  5. failure of neurotrophic mechanisms to maintain neural survival

  6. oxidative phenomena that alter the metabolism of the brain

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

Especially Alzheimer's, in particular, and dementia, in general, have an important genetic and familial component, the risk of which is increased with harmful environmental factors and/or concomitant diseases (stroke, migraine, cardiovascular disorders, high blood pressure, hypercholesterolemia and dyslipidaemias, diabetes, hypothyroidism, anaemias 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 Alzheimer's-associated neurodegeneration process. Mendelian mutations in some of these genes cause familiar forms of early Alzheimer's. Meanwhile, other genetic variants represent elements of susceptibility that increase the risk of dementia in families where these genetic defects accumulate.


A key feature of Alzheimer's is that this disease, although manifested in adult life and old age, is actually undermining the population's brain at risk since the brain stops maturing around age 30 and takes about 3 decades to give symptoms. When memory failures occur, brain damage is already so significant that conventional drug treatments are ineffective and fail to improve symptoms or disrupt the destructive process of the disease.

Alzheimer's Prevention Plan

There are currently 4 low-efficiency drugs for the treatment of Alzheimer's, developed before 2005. For the past 15 years no new drug has been approved by international regulatory agencies to treat this ailment. Defeated by the evidence, the international scientific community is concluding that the only way to defeat Alzheimer's is by intercepting the disease years before it manifests its first symptoms, for which it is urgent to put in place preventive plans to protect the at-risk population.


The International Centre for Neurosciences and Genomic Medicine, led by Dr. Ramón Cacabelos, Professor of Genomic Medicine, and internationally recognized scientist, is a global centre of reference for research into neurodegenerative diseases, with more than 1,500 scientific contributions and a vaccine (EB-101) approved by the U.S. Patent Office for Alzheimer's prevention.


EuroEspes' medical and scientific team has in recent years developed a Selective Programme for the Prevention of Dementia in the at-risk population.


Prior to participating in this medical programme, it is possible to request genetic tests, which allow us to obtain the necessary information to be able to evaluate the risk of Alzheimer's development in an individual.


This programme comprises of three different formats:

  1. Prevention Plan for first- and second-generation family members with a history of dementia in the family
  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 medical intervention model integrates:

  1. Medical examination
  2. Analytical tests (biochemistry, haematology, metabolism, neurochemistry, epigenetic biomarkers)
  3. Neuropsychological tests (cognitive and intellectual performance, emotional and behavioural 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 Ibero-American populations.

On World Alzheimer's Day the Alzheimer's Prevention Plan was launched, you can review Dr. Cacabelos' most prominent interventions and interviews in a variety of ways:

  • 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, LANE 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/ijms21093059.
  • 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 & Toxicology, 2020;16(8):673-701. DOI: 10.1080/17425255.2020.1779700.

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