Alzheimer's disease is known as a multifactorial disease. Pathological amyl
oid deposition and neurofibrillary degeneration are no longer seen as the p
rimary cause of Alzheimer's disease, but as part of a complex cascade, whic
h includes genetic risk factors, immunological disturbances, impairment of
mitochondrial metabolism, oxidative stress and formation of advanced glycat
ion end products. Pharmacological therapies based on these neurobiological
disorders offer an opportunity to improve cognitive disturbances in Alzheim
er's disease or to slow down disease progression. Several pharmacological a
pproaches to enhance cholinergic function have been developed. The second-g
eneration acetylcholinesterase inhibitors show some effect on cognition and
behavioural symptoms in Alzheimer's disease. A number of potential strateg
ies address other underlying pathological processes, including anti-inflamm
atory drugs and estrogens. Selegilin and radical scavengers like vitamins C
and E, ginkgo biloba extract and melatonin have been discovered to reduce
oxidative stress. Moreover, other approaches, such as anti-amyloids, that e
ffect secretion and aggregation of beta-amyloid as well as neurotrophic pep
tides, appear promising but are still in the early stages of development.