In addition to the cognitive effects (explained by loss of cholinergic innervation to these neuronal structures), there may also be a loss of neurovascular coupling in these regions because cholinergic-vascular innervation is reduced.

References:
Claassen JA and Jansen RW. Cholinergically mediated augmentation of cerebral perfusion in Alzheimer's disease and related cognitive disorders: the cholinergic-vascular hypothesis.J Gerontol A Biol Sci Med Sci. 2006;61(3):267-71. Abstract

View all comments by Jurgen Claassen

One of the interesting aspects of cholinergic degeneration in AD is that, although basal forebrain cholinergic neurons degenerate in AD, brain stem cholinergic neurons are basically unaffected (Woolf et al., 1989). Why might this be so? Is it due to differences in projection regions? May it be due to "intrinsic" differences in gene expression profile between these two regions? Understanding of the differences between these two regions could lead to improved therapeutic intervention targeting the affected cholinergic system. For a description of differential gene expression profiles between these two regions see a forthcoming paper in Neurobiology of Aging in which M. McKinney is senior author. (Disclosure: I am also an author of this ms.)

References:
Woolf NJ. Jacobs RW. Butcher LL. The pontomesencephalotegmental cholinergic system does not degenerate in Alzheimer's disease. Neuroscience Letters. 1989;96(3):277-82. Abstract

View all comments by Paul Coleman

There has been described a selective cholinergic alteration in the basal forebrain of AD patients and the areas innervated by these cells, mainly hippocampus and entorhinal cortex. However , tau hyperphosphorylation and amyloidβ protein accumulation seem to start in the projection areas. To me, one of the main questions in AD neurochemistry that has not been answered yet is: what is the chronological order? In other words, is the cholinergic degeneration a previous event to the posterior accumulation of neurofibrilary tangles and senile plaques? Or, on the contrary, is the cholinergic degeneration a consequence? To the best of my knowledge, there is no conclusive study to answer this important question.

View all comments by Rafael Rodríguez Puertas