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Correspondence |

Changes in PDE4D Isoforms in the Hippocampus of a Patient With Advanced Alzheimer Disease

Craig S. McLachlan, PhD, MPH; Melissa L. Chen, BSc; Clare N. Lynex, PhD; Denise L. M. Goh, MBBS, MMed; Sydney Brenner, MD, PhD, DSc; Stacey K. H. Tay, MBBS, MMed, MRCP
Arch Neurol. 2007;64(3):456-457. doi:10.1001/archneur.64.3.456.
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Alzheimer disease (AD) is associated with progressive memory decline. Memory-forming regions of the brain such as the hippocampus are potential treatment targets. Recent suggestions that cyclic adenosine monophosphate (cAMP) modulation may benefit patients with AD in preventing or delaying hippocampal memory decline1,2 remain unproven. Cyclic adenosine monophosphate is an important second messenger molecule controlling multiple cellular processes in the brain, including memory and aspects of negative mood. Levels of cAMP depend critically on phosphodiesterase (PDE) activity, enzymes responsible for the clearance of intracellular cAMP.

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