For example, transgenic mice are behaviorally abnormal from birth, so it is impossible to use these mice to determine if reducing amyloid has any beneficial cognitive or behavioral effects. Transgenic mice do not develop neurofibrillary tangles and have very limited nerve cell death, despite the accumulation of amyloid. This makes it impossible to assess the utility of reducing amyloid on other aspects of AD pathology. In a multicenter cooperative study sponsored by the National Institute on Aging, Sano et al. The combination of the two agents was not superior to either agent alone.
Cholinesterase inhibitors are the current mainstay of AD treatment.
These agents inhibit the enzyme that destroys intrasynaptic acetylcholine, thus increasing synaptic acetylcholine residence and amplifying the postsynaptic cholinergic signal. Patients may improve cognitively or experience a reduction in the rate of cognitive decline from treatment with these agents. Together, these existing and emerging therapies for AD promise to provide clinicians with an armamentarium of drugs that can meaningfully modify the course and symptoms of this illness. Dr. Cummings is Augustus S. Rose Professor of Neurology and professor of psychiatry and biobehavioral sciences at the University of California, Los Angeles, School of Medicine. References Breitner JCS, Welsh KA, Helms MJ et al.