Alzheimer’s disease (AD) is a multifactorial disorder and apparently involves
several different etiopathogenetic mechanisms. Up-to-date, there are no curative
treatments or effective disease modifying therapies for AD. A strategy to enhance the
cholinergic transmission by using acetylcholinesterase inhibitors (AChEIs) has been
proposed more than two decades ago. Food and Drug Administration (FDA) gradually
marketed these AChEIs: tacrine (1993), donepezil (1997), rivastigmine (2000) and
galantamine (2001); tacrine is no longer used because of its high prevalence of
hepatotoxicity. In addition to the AD cholinergic hypothesis , there is great evidence
that voltage-gated, uncompetitive, N-methyl-D-aspartate (NMDA) antagonist memantine
with moderate affinity can protect neurons from excitotoxicity. It was approved by FDA
for treatment of moderate to severe stages of AD in 2003. Beyond symptomatic
approaches there are anti-amyloid, neuroprotective and neuron-restorative strategies
that hold promise of redefining the course of the disease as it is known. This
contribution summarizes the main symptomatic strategies available for treating AD and
future perspectives of pharmacotherapy for improving the AD course.
