cases that remain difficult to identify upfront. One needs also to consider the plethora of central cholinesterase inhibitors already in use for the treatment of Alzheimer’s-type dementia, which act to increase central synaptic acetylcholine. Whether cholinergic neuronal replacement would ultimately prove more long-lasting and effective than small molecule cholinergic agonism remains to be established, and must be verified before transplantation of cholinergic neurons into the basal forebrains of affected patients can be reasonably considered.
