Memory disorders can derive from multicentric thalamic and cortical disease, but also from discrete structural pathology, thereby lending themselves to cell-based treatment approaches. New memory acquisition in particular may be impaired by the loss of basal forebrain cholinergic neurons projecting to the hippocampus, as well as from intrinsic hippocampal disease and disruption of the hippocampal outflow tracts. In experimental animals with disruption of the cholinergic input to the hippocampus, performance on memory tasks has responded significantly to iPSC-derived cholinergic neuronal replacement (Liu et al., 2013). That said, the common memory loss syndromes associated with early stages of Alzheimer’s and frontotemporal dementia typically herald overwhelming deterioration across all cognitive modalities as disease progression ensues; as such, isolated replacement of cholinergic neurons is likely to prove a durable clinical strategy in only very selected cases of stable or slowly-progressive memory loss – 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
