Brain cells can regenerateBMJ 1998; 317 doi: http://dx.doi.org/10.1136/bmj.317.7168.1272 (Published 07 November 1998) Cite this as: BMJ 1998;317:1272
Scientists have proved that human neurons are able to regenerate. Dr Fred Gage and colleagues at the Salk Institute for Biological Studies in California, together with doctors at the Sahlgrenska University Hospital in Sweden, have shown that new neurons do develop after birth.
This flies in the face of conventional wisdom, which suggests that brain cells, unlike all other cell types, do not reproduce.
Dr Gage's team took postmortem brain tissue from five patients who had received an intravenous injection of bromodeoxyuridine as part of their treatment for squamous cell carcinoma. This drug is a thymidine analogue and is therefore taken up into the newly synthesised DNA of dividing cells.
Because of this property, bromodeoxyuridine is sometimes used to check for tumour cell proliferation. The researchers surmised that if neurons could reproduce then any new neurons, if present, would also take up bromodeoxyuridine.
Using immunofluorescence techniques and a laser microscope, which can optically section through individual cells, the team was able to detect the presence of bromodeoxyuridine in all five postmortem specimens.
In addition to showing that new cells were present in the brain, the team also confirmed that these cells were neurons by looking for two other markers which can differentiate between neuronal cells and glial cells (Nature Medicine 1998;4:1313-7).
The brain tissue studied by Dr Gage's team comes from the dentate gyrus, the part of the brain which acts as a relay station between the cortex and the hippocampus and is important in memory and learning. As yet Dr Gage has no idea whether the new cells identified in these sections are fully functional or under what sort of conditions new cells would be introduced. “There may be a replacement phenomenon going on, but we have no clear answer as to whether or not there is cell death over time,” he said.
Plasticity and autologous repair may also have to be re-examined in the light of these findings.
In diseases such as Alzheimer's, Parkinson's, and multiple sclerosis, neuronal death obviously occurs, but there may be something about the disease process itself that prevents what might now be considered “normal” neurogenesis from taking place.
Clearly, the factors that stimulate and limit neurogenesis will have to be better understood before any mechanisms for slowing or reversing neuronal loss can hope to offer benefit to people with these neurodegenerative diseases.