Alzheimer’s Disease

Tau and Beta – amyloid are 2 proteins known as cerebral plaque slowing down neuro transmitters. This causes lapses of memory which become more and more frequent until the patient is incapable of taking care of himself. AA7 is designed to clear this plaque freeing up the neuro transmitters and regaining the patients access to his memory.

Background

Alzheimer’s disease (AD), also known as just Alzheimer’s, is a chronic neurodegenerative disease that usually starts slowly and gets worse over time. It is the cause of 60% to 70% of cases of dementia. The most common early symptom is difficulty in remembering recent events (short-term memory loss). As the disease advances, symptoms can include problems with language, disorientation (including easily getting lost), mood swings, loss of motivation, not managing self-care, and behavioural issues. As a person’s condition declines, they often withdraw from family and society. Gradually, bodily functions are lost, ultimately leading to death. Although the speed of progression can vary, the average life expectancy following diagnosis is three to nine years.

Observational Studies

Alzheimer’s disease has been identified as a protein misfolding disease (proteopathy), caused by plaque accumulation of abnormally folded amyloid beta protein, and tau protein in the brain Cesa developed a molecule that targets both Amyloid and Tau. First short term (4 weeks)  observational studies on advanced (stage 5+) AD patients showed a rapid regeneration of short term memory and formed the basis for an official placebo controlled clinical trial.

Clinical Trials

At the moment a small pre-clinical placebo controlled trial study is being performed on stage 3-4 ( Medium) Alzheimer patients. Intermediate results show already a 20% improvement on the cognitive abilities. After 6 months the group will be unblinded and the report published. Based on the experiences of this small trial a major multi-location Placebo controlled Clinical trial will be started in Spring 2018.