February 16, 2011
Increasing Brain Enzyme May Slow Alzheimer’s Disease Progression
LA BioMed study finds damaging accumulation of tau proteins removed
Increasing puromycin-sensitive aminopeptidase, the most abundant brain peptidase in mammals, slowed the damaging accumulation of tau proteins that are toxic to nerve cells and eventually lead to the neurofibrillary tangles, a major pathological hallmark of Alzheimer's disease and other forms of dementia, according to a study published online in the journal, Human Molecular Genetics.
"Our research demonstrated that increasing the brain enzyme known as PSA/NPEPPS can effectively block the accumulation of tau protein that is toxic to nerve cells and slow down the progression of neural degeneration without unwanted side effects," said Stanislav L. Karsten, PhD, the corresponding author for the study and a principal investigator at Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center (LA BioMed). "These findings suggest that increasing this naturally occurring brain peptidase, PSA/NPEPPS, may be a feasible therapeutic approach to eliminate the accumulation of unwanted toxic proteins, such as tau, that cause the neural degeneration associated with the devastating effects of Alzheimer's disease and other forms of dementia."
Alzheimer's disease affects 2 million to 4 million Americans, and their ranks are expected to grow to as many as 14 million by the middle of the 21st century as the population ages.
The potential for PSA/NPEPPS to protect neurons from degeneration was first reported in a 2006 issue of the journal, Neuron. At that time, researchers hypothesized that PSA/NPEPPS may be a natural mechanism for protecting neurons. Dr. Karsten, who was the lead author of the 2006 study, said the new study is the first to provide the data confirming the neuroprotective role of PSA/NPEPPS in mammals.
On the Net:
- Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center (LA BioMed)
- Human Molecular Genetics