New Vaccine Could Prevent Alzheimer’s Disease Progression

Aging is considered a most important risk factor for the Alzheimer’s disease. Recently, reports support a theory that the therapeutic immunomodulatory vaccine has the potential to be safer for age-associated decline in immunity.

A team of neuroscientist at the University of South Florida (USF Health) found in their preclinical study that an “antigen-presenting dendritic vaccine” develops a specific antibody immune response to oligomeric Aβ. Therefore, it is suggested that it may be safer and caters benefits in treating Alzheimer’s disease in clinical setting.

In the study, neuroscientists used the specific immune cells called dendritic cells which are loaded with a modified A beta peptide as the antigen in the vaccine formulation. Research findings are published in the Journal of Alzheimer’s Disease.

Human immune system has the capacity to develop a well-organized immune response against foreign invading substances, including toxins. However, it gradually weakens with increasing age, resulting in reduced efficacy in vaccines in people over age 65. Recent reports propose a theory that immunotherapy targeting the neurotoxic forms of the “peptide amyloid beta (oligomeric Aβ)” may prevent the diseases progression, particularly the most common age-related neurodegenerative disease.

Recent data indicates that one of the fundamental factors of causing a disease is hardened deposits of Aβ that aggregates and clump together between nerve cells resulting in formation of “amyloid protein plaques)” in the brain. This thereby led to damaged neurological cell signaling, ultimately causing the onset of Alzheimer’s disease and symptoms.

Source: CDC

The preclinical study this investigational vaccine on Alzheimer’s was conducted on a mouse model by Dr. Cao and colleagues, used the “next-generation anti-amyloid E22W42 DC vaccine” used dendritic immune cells (DC) that were loaded with a modified Aβ peptide as the antigen. It was proved in the study that it would profoundly produce a long-lasting immune response where a moderate level of antibody will be required to prevent the aggregation of Aβ oligomers into destructive Alzheimer’s plaques. According to Dr. Cao, it will consequently activated the immune system moderately without over-activation of the immune systems in elderly people.

Dr. Cao, a neuroscientist at the USF Health Taneja College of Pharmacy, USF Health Morsani College of Medicine and the university’s Byrd Alzheimer’s Center, said, “This therapeutic vaccine uses the body’s own immune cells to target the toxic Aβ molecules that accumulate harmfully in the brain.”

In this study, the researchers used bone marrow of mouse model to extract the dendritic cells, then formulated using modified Aβ-sensitized with dendritic cells. The study recruited three groups of mouse models that were given different formulations: first transgenic was given the investigational E22W42 DC vaccine, second wild-type vaccine transgenic group received “endogenous amyloid beta peptide” to stimulate the dendritic cells, the third DC control transgenic group was injected with dendritic cells only with no Aβ peptide, and a fourth non-transgenic control group included untreated healthy and older mice.

The results showed that in transgenic mice with Alzheimer’s from the E22W42 DC-vaccinated group, less memory impairment was found and significantly less errors were observed in working memory, compared to mice DC controls.

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