Targeting JNK for the diagnosis and treatment of Alzheimer's disease

Abstract

Alzheimer's disease (AD) affects over half million people in Spain and it is estimated that there are two million people directly related to the disease. Although AD etiology is still unknown, it seems is to be associated to neuronal apoptosis and synaptic terminals loss, resulting in neuroinflammation and neurodegeneration. In this context, different studies have shown the MAPK pathways involvement, such as JNK, in neuronal death and neuroinflammation. Evidence indicates that JNK cascade is activated in several experimental models of AD and its over-activation is related to AD pathology, such as maturation of neurofibrillary tangles and plaque formation senile. Last years, JNK inhibitors, omega 3 fatty acids (ù-3 PUFAs) among them, seem to have a potential development in clinical trials for different indications. Several studies and clinical research have suggested beneficial effects of marine omega 3 (ù-3 PUFAs) on neurodegenerative diseases, specifically EA. The ù-3 PUFAs therapeutic actions seem to be related to the resolution of neuroinflammation characteristic of AD. Although the beneficial effects of ù-3 PUFAs have been demonstrated in experimental models, the therapeutic effect in clinical trials is controversial. Therefore, it is suggested to study JNK pathway as therapeutic target or as complementary strategy to reduce pathological processes of AD.