Alzheimer's

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.