The study was performed by researchers from the Medical University of South Carolina (MUSC) and Beth Israel Deaconess Medical Center (BIDMC), Harvard Medical School. The team observed signs of brain inflammation and memory loss in a pre-clinical model of vascular dementia (VaD) and severe cognitive impairment in a separate pre-clinical model of Alzheimer’s disease (AD).
‘cis P-tau mAb reversed 85% to 90 % of the severe clinical features of dementia.
A toxic, non-degradable version of a healthy brain protein called cis P-tau was associated with both cases. When treating the mice (pre-clinical models) with the monoclonal antibody (mAb) cis P-tau mAb, the team obtained promising outcomes in preventing clinical features like neural degradation and cognitive decline.
The changes caused by the accumulation of cis P-tau protein in the genetic architecture of the VaD model were also consistent with those seen in human AD patients.
The team ultimately showed that therapy using cis P-tau mAb reversed 85% to 90 % of above mentioned clinical features.
“We believe our findings have not only discovered cis P-tau as a previously unrecognized major early driver of VaD and AD but also identified a highly effective and specific immunotherapy to target this common disease driver for treating and preventing AD and VaD at early stages,” said Onder Albayram, Ph.D., co-lead author and assistant professor in the Division of Cardiology in the Department of Medicine at MUSC.