In Alzheimer's disease, the cholinergic septal input to the dentate gyrus molecular layer appears to sprout, presumably in response to the loss of entorhinal input to this region. Neuritic plaques accumulated in regions of septal sprouting and were present in these regions to a much greater degree than in areas of no apparent sprouting. We suggest that the reactive sprouts participate in the pathogenesis of plaque formation. The stimulus for plaque formation may be sprouting induced by a focal accumulation of injury-induced trophic factors. The demonstration of sprouting in Alzheimer's disease indicates that the appropriate mechanisms are intact. Eventually, however, the fibers succumb to the pathogenic processes in the disorder.
|Number of pages||10|
|State||Published - Dec 1986|
Bibliographical noteFunding Information:
Abbreviations: AChE-acetylcholinesterase, AD-Alzheimer’s disease. ’ The authors thank Ron C. Kim, Helena Chang Chui, ha T. Lott, Byung Choi, and Ursula T. Slager for clinical and neuropathological evaluation. We also thank Mark A. Borja and Suzanne M. Cooper for technical assistance. This work was supported by NIA program project AGO0538 and ADRDA Grant B-86-102. K.J.A. is the recipient of a postdoctoral fellowship from the National Institutes of Health (NS07627).
ASJC Scopus subject areas
- Developmental Neuroscience