3% to 28.4%. [18F]FDG PET contributed more to the improvement in the accuracy than CSF or MRI, showing the usefulness of molecular learn more imaging in the early diagnosis of AD.169 Current drugs for AD include acetylcholinerase inhibitors such as donepezil and rivastigmine; memantine, a drug that blocks NMDA receptors,170 and drugs that combat the neurotoxic effect of Aβ plaques including the

L-type calcium channel antagonist nimopidine, and antioxidants such as vitamin E.171 Candidate drugs Inhibitors,research,lifescience,medical for AD include beta and gamma secretase inhibitors, and immunogenic synthetic Aβ42 or monoclonal antibodies (eg, bapineuzumab) against Aβ42.172 Molecular imaging is not only useful for the early detection

Inhibitors,research,lifescience,medical of AD and MCI, but also for predicting treatment response to anti-amyloid and other drugs, and may serve as a surrogate outcome measure.172,173 For example, some PET studies reported reduction of brain Aβ plaques measured by [11C]PIB after the treatment with Inhibitors,research,lifescience,medical anti-amyloid agents, though the disease modifying effects need further confirmation.174-176 The imaging of inflammatory mediators such as microglia may help assess the effectiveness of drugs that are targeted toward reducing inflammation in the brain, such as NSAIDs. Moreover, since abnormalities in cholinergic, noradrenergic, serotonergic,

and dopaminergic Inhibitors,research,lifescience,medical systems are all thought to contribute to AD pathophysiology, imaging of these neurotransmitter systems will help develop further drug targets and evaluate their efficacy.173 Conclusions How molecular imaging has uniquely changed thinking about these illnesses Molecular imaging enables molecular processes to be related to the clinical presentation, and subsequent course of CNS disorders. Inhibitors,research,lifescience,medical For example, in the case of schizophrenia it has provided data on the regional nature of the dopamine alterations in the brain at the onset, and even predating the illness. Furthermore, molecular imaging has narrowed down the nature of the dopaminergic alterations at onset of the disorder- identifying that the major alterations are presynaptic and not at the receptor or transporter level- and tuclazepam related this to subsequent clinical outcomes. This has enabled the dopamine hypothesis of schizophrenia to be revised in ways that would not have been possible with other techniques. Molecular imaging also clarified how antipsychotics work — demonstrating that D2/3, but not D1 or 5-HT2A, receptor occupancy is linked to subsequent treatment response and side effects. This finding has contributed to a change in clinical practice away from the use of high dose antipsychotics towards lower doses.