New Research Areas

Multiple strategies for AD treatment have emerged from an evolving understanding over the past 10-20 years regarding the pathological basis of the disease. The limited time window for effective symptomatic treatment with AChE inhibitors observed in clinical practice in patients with mild to moderate AD highlights the need for additional treatment strategies. Memantine was a partial solution to this need in treating later AD stages (i.e., moderate to severe). Other AChE inhibitors (e.g., TAK147 7, CHF2819 8, huperzine A 9) that have improved CNS selectively are in clinical trials with slow progress. AChE also appears to have alternate activities beyond catabolism of ACh, including accelerating the rate of formation of Ab fibrils, and inhibitors that affect both activities are under development,34 including analogs of phenserine 10.35

Since cholinergic afferent neurons projecting to the basal forebrain and hippocampus are lost in AD, agonists that stimulate ACh release by interaction with presynaptic receptors and also mimic ACh to stimulate postsynaptic receptors (i.e., mAChRs and nAChRs) and facilitate neurotransmission have been investigated as therapeutic treatments. NCEs that target these postsynaptic ACh receptors in theory would serve as add-ons to AChE inhibitors. Strategies to halt disease progression include targeting production, aggregation, and clearance of Ab, hyperpho-sphorylation of tau, and neuroinflammation, all of which are key elements leading to neuronal dysfunction and cell death. Multiple strategies to block neuronal death via trophic support or by interfering with death signaling pathways are also being explored and a host of targets that facilitate improvements in cognition are under investigation.

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