Increasing brain enzyme may slow Alzheimer's disease

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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, as per a research studypublished online in the journal, Human Molecular Genetics

Stanislav Karsten, an LA BioMed principal researcher, is the lead author of a new study on Alzheimer's disease.

Credit: LA BioMed


Scientists found they could safely increase the puromycin-sensitive aminopeptidase, PSA/NPEPPS, by two to three times the usual amount in animal models, and it removed the tau proteins in the neurons. Removing the tau proteins restored neuronal density and slowed down disease progression. Scientists detected no abnormalities caused by the increase in PSA/NPEPPS, suggesting that elevating PSA/NPEPPS activity appears to be a viable approach to treat Alzheimer's disease and other forms of dementia, known a tauopathies.

"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, appears to be a feasible therapeutic approach to eliminate the accumulation of unwanted toxic proteins, such as tau, that cause the neural degeneration linked to 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 a number of 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, scientists hypothesized that PSA/NPEPPS appears to be a natural mechanism for protecting neurons. Dr. Karsten, who was the main author of the 2006 study, said the newly released study is the first to provide the data confirming the neuroprotective role of PSA/NPEPPS in mammals.


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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, as per a research studypublished online in the journal, Human Molecular Genetics