ABSTRACT
Alzheimer’s disease (AD) is a neurodegenerative condition characterized by the presence of neurofibrillary tangles together with the accumulation and extracellular deposition of amyloid-beta (Aß) peptide in the form of senile plaques. In addition to these hallmarks, profound neuron loss and infiltration of inflammatory cells are also observed. The precise role of inflammation in AD has been widely debated. Early on, microglia and astrocytes were shown not only to increase the production of Aß peptide but also to induce an inflammatory autotoxic state. Aß peptide, produced from the processing of the amyloid precursor protein, exists in various oligomeric forms and ultimately assembles into fibers. A major task would be to develop an inhibitor specific to this cerebral isoform of cAMP-Specific Phosphodiesterase 4B (Pde4B) thus avoiding the serious side effects that have been described for some Pde4B inhibitors.
