Nucleus Basalis Lesions and Recovery

Since the early reports of cortical cholinergic deficits in Alzheimer’s disease (AD) and loss of cholinergic cells in the basal forebrain a great deal of research effort has been directed towards strategies to affect recovery from the consequences of cholinergic deficits. Nucleus basalis of Meynert (nbM) lesions in non-human mammals have been found to consistently produce dramatic deficits in cortical cholinergic marker activity, as well as profoundly disrupting learning and memory functions (Olton and Wenk, 1987). Recovery of function at a neurochemical as well as a behavioral level has been demonstrated in animals with such lesions. Evidence can be cited for spontaneous, as well as experimentally induced recovery. Recovery from nbM lesions, and basal forebrain cholinergic systems can most readily be induced experimentally. In general, recovery has been induced by pharmacological or neurotrophic means.