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Int Psychogeriatr. 2003 Sep;15(3):223-37.

Toward an early diagnosis and treatment of Alzheimer's disease.

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Karolinska Institutet, Neurotec Department, Division of Molecular Neuropharmacology, Huddinge University Hospital, Stockholm, Sweden.


Alzheimer's disease (AD) is the most common neurodegenerative disease. There has been a rapid increase in the knowledge of epidemiology, genetics, risk factors, and underlying neuropathological mechanisms, but still there is no cure for AD. Recent promising studies with functional imaging using positron emission tomography (PET) and magnetic resonance imaging reveal that disease processes can be detected when very early subjective symptoms of AD are manifest. Recently the PET ligand PIB was reported to bind in vivo to beta-amyloid in the brains of AD patients. Also cerebrospinal fluid markers including tau, phosphotau, and A beta 1-42 are probably important early biological markers that will provide an early diagnosis of AD. An obvious impairment in central cholinergic transmitter function and its close relation to cognitive function led to the development of the acetylcholinesterase inhibitors that now are used as symptomatic therapy. A drug interfering with the glutaminergic brain transmitter system, the NMDA antagonist memantine, has recently been approved for the treatment of patients with severe AD. In order to stop or reverse disease progression, different AD treatment strategies are of great interest. Epidemiological studies support the hypothesis that long-term treatment with estrogen, antioxidants, anti-inflammatory drugs, and cholesterol-lowering agents could protect against the development of AD. Treatment with these drugs in manifest AD has been less promising. The use of nerve growth factors was limited by severe side effects. Much evidence supports the key role of beta-amyloid in the pathogenesis of AD. Compounds such as amyloid beta-sheet breakers, cholesterol-lowering drugs, estrogen, nicotine, zinc and copper chelators, inhibitors of beta- and gamma-secretases, and immunization to reduce the amyloid burden in transgenic mice overexpressing beta-amyloid all have their advocates. The latter exciting strategy turned out to cause meningoencephalitis in 6% of AD patients so treated. One patient from the trial has died showing less beta-amyloid burden in brain than expected and patients with serum beta-amyloid plaque reactive antibodies had less cognitive decline after 1 year than AD patients without antibodies. There is a great optimism for early diagnosis and effective treatment of AD in the future.

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