The research out there on neural regrowth in adults is very interesting, because, yes, the classical empirical evidence is that damaged neurons go into apoptosis and are cleaned up by glial cells.
My girlfriend has atypical trigeminal neuralgia and underwent an unsuccessful microvascular decompression on the brainstem (wherein a venous structure was deconstructed and cauterized, a venule was padded with teflon, and a minor arteriole was resectioned and cauterized), followed by a more-successful partial sensory rhizotomy to resection the nerve in Meckel's cave via a 60% cut that ideally would hit most of the group-C fibers. The outcome of the rhizotomy is interesting, because it seemed to take care of the mandibular nerve pain while leading to a very odd outcome. In the vast, vast majority of partial sensory rhizotomies on cranial nerves (meaning more-or-less the ~99% who do not have the horrid-sounding outcome known as anaesthesia dolorosa), the loss of sensation eventually diminishes, as the nerve undergoes restructuring. There seems to be very little information in popular medical literature on the restructuring process, and as I don't have access to any specialized journals (for neurology, neurosurgery, etc.), I cannot find much information; however, it seems to perhaps involve rapid branching of the dendrites in parallel with apoptosis and glial clean-up of damaged neurons. In >90% of rhizotomies, there is little discomfort during this process. My girlfriend is one of the "lucky few" (and by that I mean that her neurosurgeons, Dr. Sekula and Dr. Jannetta, who himself pioneered microvascular decompression and other techniques for trigeminal neuralgia of both types and various types of hemifacial spasm, at Allegheny General Hospital, said they could not even remember the last time they had seen the effect she is experiencing) to have severe discomfort during the restructuring process. This discomfort is a dysthesia characterized by intense sensations of all types from the cranial nerve. She is experiencing sensations of pressure, nociception, touch, and proprioception in all branches of the trigeminal nerve, meaning not only the major three branches (ophthalmic, maxillary, and mandibular), but the minor branches out of Meckel's cave as well. In addition to that, she is having branching across into adjacent cranial nerves. These sensations range from moderately intense to maximally intense (meaning she is experiencing at times the same sensations someone would have if their skull was being crushed to pulp, or face was being cut deeply open in many places, etc.), but at least they can be controlled somewhat by extremely high levels of antiseizure medication. Between the sensations and medication, though, she is effectively completely disabled while the nerve undergoes this type of healing. The good news is that her neurosurgeons have never seen, either themselves or in any journals, a case of this that does not resolve when the restructuring reaches its end-stage, which occurs after six to twelve months. The intermediate time, though, is Hell for her. I would love to see more research done on this, as I would be curious to see if various signalling mechanisms are not genetically nominal in the <10% of cranial nerve rhizotomy patients who have this type of post-procedural effect.
Please, let's continue the research on SOCS3 here, and the other research being done out there on the various other known signalling mechanisms.