Amyloid Beta Nano Particle used to Sensitize Dendritic Cells as a Therapeutic Vaccine against Alzheimer's disease

The annual cost of Alzheimer’s Disease (AD) is approximately $230 billion and it is estimated that the incidence of AD will increase three-fold if there is still no solution by the year 2050. Thus, there is a desperate need to develop and implement effective strategies for AD. Until now, FDA approved drugs could only temporally improve memory by increasing the neurotransmitters in the brain by inhibiting either the acetylcholine esterase activity or NMDA receptor. Therefore, results from data of all FDA approved drugs show that they could not stop or slow down the disease progress at all. Since Aβ accumulation and Tau phosphorylation are considered to be the major pathological factor, immunotherapy against pathological factors such as Aβ and Tau have emerged in the past 16 years.  There has been evidence suggesting that an active vaccination strategy targeting the amyloid beta (Aβ) protein (i.e. Aβ 1-42) may have some efficacy, as stated by studies in a transgenic mouse model for AD. The history of immunotherapies against AD reveals that AD patients are old subjects with deteriorated immune systems, so a normal vaccine strategy will not work on this population unless strong adjuvants are used to stimulate and over prime the immune system. However, such adjuvants will lead to over-activation of the immune system that induces an unwanted response. On the contrary, the passive immunotherapy relies on infused antibody, and antibody will not be able to have immune activate effects, so it will not be proper for long-term treatment for AD patient. Thus, the best approach for effectively dealing with AD must be able to simultaneously target the pathological factor and address the impaired immune system for a longer period time. This can be achieved by using dendritic cells obtained from the patient and sensitizing the cells with a mutated form of Aβ. This allows for the subject’s immune system to target the aggregated Aβ, therefore reducing the symptoms of AD.