Dr Ramón Cacabelos, Professor and Chairman of Genomic Medicine, announces the implementation of a Preventive Program for Alzheimer’s disease at the International Center of Neurosciences and Genomic Medicine, Corunna, Spain.
Alzheimer’s disease (AD) is a major problem of health in developed countries, with a great psychosocial and socioeconomic health impact. AD is the main cause of dementia (> 50%), followed by vascular dementia, mixed dementia and other forms of progressive, irreversible neurodegeneration.
AD is a multifactorial / complex disorder in which genomic defects, epigenetic aberrations, cerebrovascular damage and environmental risk factors pathogenically converge to induce premature neuronal death. With a prevalence ranging from 1.8% at 65-69 years to 42.1% at age 95-99 years (annual incidence of 34.1 per 1,000 persons >60 years) and an age-adjusted death rate of 25.4 per 100,000, AD is the most important neurodegenerative disorder worldwide, contributing to disability and high socioeconomic burden. Assuming an average annual cost per patient of $15,000-20,000, a conservative analysis would estimate a global cost worldwide of over $700 billion.
AD neuropathology is characterised by the presence of extracellular deposits of β-amyloid in senile plaques and intracellular neurofibrillary tangles formed by hyperphosphorylation of the Tau protein, which reflects alterations in the cytoarchitecture of neurons. These neuropathological hallmarks are accompanied by dendritic branching and neuronal loss. At the clinical level, AD patients show progressive cognitive deterioration, behavioural changes and functional decline, with an average half-life from disease onset to death of 6-12 years, depending upon the age at onset and concomitant health conditions.
Alzheimer’s disease is a complex and multifactorial disease caused by (i) multiple defects in the human genome, (ii) epigenetic aberrations that alter the normal expression of genes, (iii) cerebrovascular alterations responsible for the lack of cerebral oxygenation, (iv) neuroinflammatory and cytotoxic reactions, (v) failure of neurotrophic mechanisms to maintain neuronal survival, (vi) oxidative phenomena that alter brain metabolism, and (vii) a multitude of environmental processes that cause brain damage (microtrauma, toxic substances, inadequate drugs, poor nutrition).
Dementia in general and AD, in particular, have an important genetic and family component, whose risk is increased with pernicious environmental factors and / or concomitant diseases (stroke, migraine, cardiovascular disorders, high blood pressure, hypercholesterolemia and dyslipidemia, diabetes, hypothyroidism, anaemias and deficiency syndromes associated with folic acid and vitamin B12 deficiencies).
There are more than 600 genes distributed across the human genome whose mutational defects or alterations in gene expression contribute to the neurodegenerative process associated with AD. Mendelian mutations in some of these genes cause familial early-onset AD, and other genetic variants of susceptibility increase the risk of suffering dementia in those families where these genetic alterations accumulate.
A fundamental characteristic of Alzheimer’s disease is that, although it appears in adult life at an old age, it is really undermining the brain of the population at risk since the brain stops maturing around the age of 30 and takes about 3 decades to develop symptoms. When memory failures appear, brain damage is already so significant that conventional pharmacological treatments are ineffective and fail to improve symptoms or halt the neuro-destructive process of the disease.
During the period 1993-2003, the current anti-AD drugs (Tacrine, Donepezil, Rivastigmine, Galantamine, Memantine) were introduced in the market, and since then no new drugs for AD have been approved by the health authorities. Approximately 10-20% of the total cost of dementia is due to pharmacological treatment; however, current drugs are not cost-effective and most of them are not devoid of adverse drug reactions and drug-drug interactions in a fragile population of patients under age- and pluri-pathology-related polypharmacy.
Overcome by the evidence, the international scientific community is coming to the conviction that the only way to effectively fight AD is by intercepting its destructive neurodegenerative process years before the development of clinical symptoms. With this purpose, it is essential to implement preventive programs for halting disease progression in very early stages of the disease, especially in the population at risk.
The International Center for Neurosciences and Genomic Medicine, directed by Dr Ramon Cacabelos, Professor and Chairman of Genomic Medicine and recognised scientist in the international arena, is a world reference centre in Neurosciences, with more than 1,500 scientific contributions and a vaccine (EB -101) approved by the United States Patent Office for Alzheimer’s prevention.
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. This program includes 3 modalities: (i) Prevention Plan for first and second-generation relatives of patients with a family history of dementia; (ii) Prevention Plan for people with cardiovascular and / or cerebrovascular diseases, that represent risk factors for vascular and / or mixed dementia, or subjects with a family history of cerebrovascular disorders (ie stroke) or vascular dementia and (iii) Dementia Prevention Plan for the general population.
The medical intervention model integrates (i) medical examination, (ii) analytical tests (biochemistry, haematology, metabolism, neurochemistry, epigenetic biomarkers), (iii) neuropsychological tests (cognitive and intellectual performance, emotional and behavioural status, psychomotor function), (iv) static and functional neuroimaging with state-of-the-art neurotechnology, (v) predictive and pathogenic genomic analysis, and (vi) personalised preventive and / or therapeutic interventions based on individual pharmacogenomics protocols.