NEUROBIOLOGY. In the article “Age-associated neuronal atrophy occurs in the primate brain and is reversible by growth factor gene therapy” by D. E. Smith, J. Roberts, F. H. Gage, and M. H. Tuszynski, which appeared in number 19, September 14, 1999, of Proc. Natl. Acad. Sci. USA (96, 10893–10898), the authors want to note that (i) due to a printer’s error Fig. 1 was reproduced smaller than requested and (ii) that the equation on page 10894 is incorrect. The corrected equation and figure are shown below:

Figure 1.

p75 immunolabeling in aged and nonaged monkeys. (a) Ch4i region in nonaged monkey exhibits normal distribution of cholinergic neurons. Ch4id: Ch4 nucleus, intermediate-dorsal component; Ch4iv: Ch4 nucleus, intermediate-ventral component. M, medial. Bar = 450 μm in a–d. (Inset) Normal p75-immunolabeled neurons and neurite density at 20-fold higher magnification. (b) Ch4i region in aged nongrafted monkey, showing fewer neurons that appear more pale than those of nonaged subjects. Inset indicates lower neuronal and neurite density than observed in nonaged monkey. (c) In contrast, p75-labeled neurons in monkeys with control grafts exhibit no evident morphological response to the adjacent graft. Neurons resemble those of nongrafted aged subjects in extent of loss of neuronal labeling and neurite density. (d) Ch4i region in aged NGF-grafted monkey shows restoration of neuronal and neuritic density. NGF-secreting fibroblast graft (G) is dark because of dense penetration by p75-labeled cholinergic axons. Many neuronal soma orient in the direction of the NGF-secreting cell source and extend axons into the graft. Inset demonstrates these changes at 20-fold higher magnification.