Research published in 1998-1999 in Nature Medicine & in 2006 in Nature Neuroscience, Schwartz’s team set the ground for a new notion that had never been tested or even suggested before:
The brain needs the immune system for its maintenance. As the immune system weakens with age, the communication between the brain & immune system is compromised, accelerating dementia & Alzheimer’s. 
“Common wisdom for decades has been that the brain is completely isolated from the immune system,” Schwartz said.
“What my team suggested in the 1998 & other follow-up studies was that the brain actually does need the help of immune cells to keep healthy & that the aging of the brain & Alzheimer’s is associated with this insufficient communication between the brain & immune system.” 
“If the immune system prematurely ages it causes loss in cognitive performance,” she added.
“The integrity of the immune system is needed for brain support, for supporting brain plasticity & repair.” 
Armed with this knowledge, the team set out to show that if communication between the immune system & brain is restored, “we can modify or change the course of Alzheimer’s disease.” 
Releasing the immune system’s ‘brakes’ -
The key was to find a way to boost the immune system in a controlled way, to restore communication & thereby to help mobilize the relevant immune cell population from the periphery to the brain, Schwartz said. 
The researchers did this by using an antibody that would release the immune system’s “brakes” so it could start once again communicating with the brain.  The brakes within the immune system cells keep the immune system under control.
With the aging process, the brakes tend to become over-controlling, suppressing the immune system too much, which causes ”an exhaustion of the immune system,” Schwartz explained. 
“Rather than trying to deal directly with the plaques or any waste accumulated in the brain in this disease, we believe that if we boost the immune system, we re-activate a mechanism of maintenance & repair,” she said. 
The antibody IBC has engineered, based on the new understanding, has the ability to neutralize “1 of the mechanisms that keeps the immune system under tight control,” Schwartz said.
“The key is to release such brakes modestly, at an optimal level,” in order to avoid the side effects of overactivation. 
In the lab, using animal models with Alzheimer’s disease & dementia, the treatment with such antibody showed a “robust improvement in cognition & a reduction of the pathology,” she said.
The effect was noticed on all the multiple toxic compounds that were built up in the brain, “thus addressing the multi-factorial nature of the diseases & their heterogeneity among patients,” Schwartz explained.