Alzheimer disease and neuroplasticity: New approaches and new targets in pharmacotherapy

Alzheimer disease (AD) is the major cause of dementia in the aged individuals. It is a neurodegenerative disorder characterized by apoptosis and loss of neurons resulting in synaptic dysfunction in central pathways involved in learning and memory. Neuroplasticity can simply be defined as changes in the brain neurons, and structural and functional changes in synapses formed by these neurons. If the changes are not confined to a single neuron but reach the level of a synapse the adaptive response formed may also be called “synaptic plasticity”. Brain is adapted to all exogenous and endogenous stimulations (i.e. environmental or emotional stresses) by neuroplasticity. The most essential statement on AD pathology is that it assault the processes associated with neuroplasticity in central nervous system (CNS). Directly focusing on the causes of damages of synaptic elements and development of new therapeutic approaches devoted to reverse impaired neuroplasticity induced by the disorder may be a more effective strategy and provide more consistent solutions in the treatment of AD. The main objective of this review article is to update our knowledge on AD in the light of the present literature and discuss the new approaches and targets such as neuroplasticity hypothesis of AD and new candidate drugs.