Could This be the Era of a Solution to Alzheimer's?

Recent scientists have discovered an antibody, Aducanumab, as well as a crucial protein in adult neuroplasticity, Reelin, that reduce the effect of harmful amyloid-beta plaques in Alzheimer's patients.

Alzheimer's disease is characterized as a progressive neural degenerative disorder that destroys memory and causes problems with vital mental functions such as behavior, cognitive deficits, difficulty with language, calculations, and visual-spatial skills. Unfortunately, Alzheimer's disease is the most common form of dementia, serious enough to interfere with daily life and has no known cure or effective treatment. It's greatest known risk factor is increasing age, with a current number of 5.3 million patients in the United States alone with data showing 6-8% of individuals over the age of 65 and 40% above the age of 85.

The two pathological causes that have been much researched as the potential sources of this disease are the production of neurofibrillary tangles and extracellular deposits of protein amyloid beta plaques. fMRI analysis have revealed that the progression of Alzheimer's starts with a massive degeneration beginning from the hippocampus (the main center for memory). The disease typically then proceeds by spreading degeneration to near by areas such as the language cortices and more; typically sparing the motor cortices. This degeneration leads to ventricular enlargement and a whole system atrophy, effecting the individuals behavior, cognition, memory, and overall mental health.  

In Dr. Sisodia's molecular neurobiology research on amyloid beta plaques, he discusses his research on the antibody Aducanumab as well as it's result on almost complete clearance of the amyloid-beta plaques in the study group of patients with early-onset Alzheimer's post-treatment administration. He tells us in his research that although the causes of the disease are still unknown, it is clear that it commences with the progressive amyloid deposition in the brain of affected individuals between 10 to 15 years before the emergence of any initial clinical symptoms such as memory loss. The recent finding of the Aducanumab antibody haults/significantly slows down the process of the amyloid deposition before further cognitive degeneration could occur. To do this, the human monoclonal antibody, Aducanumab, selectively binds to brain amyloid plaques, thus enabling microglial cells for the plaques removal. After one year of treatment, practically no beta-amyloid plaques were detected in the patients who had received the highest dose of the antibody. The cognitive results were evaluated by a standardized questionnaire to assess individual's cognitive abilities and everyday activities of the patients. "While patients in the placebo group exhibited significant cognitive decline, cognitive ability remained distinctly more stable in patients receiving the antibody" (Sevigny). The treatment of this anti-body therefore demonstrates a significant reduction of the progression of the disease, a huge microbiological step for success in prevention of Alzheimer's.

The critical difficulty with this treatment is being able to find individuals very early in their onset, in order to stop progressive cognitive decline before symptoms become dramatic. This issue has had the same result in a second study from the University of Barcelona that uses Reelin, a synaptic cognitive enhancer as well a as crucial protein in adult neuroplasticity in genetically mutated mice. In the results from researchers Daniela Rossi, Lluis Pujadas, Eduardo Soriano and Natalia Carulla, they found that Reelin has a neuroprotective effect in neurodegenerative diseases. This brain plasticity promoter protein can rescue an Alzheimer's clinical phenotype in the mouse animal model by cognitive deficits recovery, which take place after the activation of the Reenal signaling pathway. This signaling pathway homeostatically regulates global neuronal function in cognition, neuronal plasticity, amyloid formation and more. Soriano stresses that this methodological approach on signaling pathways which control different features related to brain plasticity and Alzheimer's disease is an effective technique in comparison to other studies that focused more on lessening the symptoms, a similar technique used when discovering the effects of Aducanumab anti-body. The over expression of Reelin may be beneficial to reduce the amyloid plaque formation as well as the neuroprotective effect of being a synaptic and cognitive enhancer to regulate the precursor of amyloid beta. Although this research has only been proved in invivo animal models and has not yet been attempted on humans and is said to deserve consideration as a therapeutic target for the treatment of Alzheimer's disease pathogenesis as are the findings of the Aducanumab protein.

Both of these research findings explore the microbiological approach to solving the onset of disease as opposed to regulating it's symptoms. By enhancing detectability, we can apply these new discoveries early-on in the disease in order to prevent the maturation of the condition for individuals around the world, eventually dramatically lowering it's effect by preserving patients cognitive function. Together, these two findings are paving the way to solving the degenerative mysteries that could potentially solve and cure the widespread occurrence and effects of Alzheimer's disease. 

References

Sevigny, Jeff, Ping Chiao, Thierry Bussiere, Paul H. Weinred, Leslie Williams, Marcel Maler, and Robert Dunstan. "The antibody aducanumab reduces Aβ plaques in Alzheimer’s disease."Nature537 (2016): 50-55. Web. 29 Apr. 2017.

Universidad de Barcelona. "Reelin protein rescues cognitive deficits in an animal model of Alzheimer's disease." ScienceDaily. ScienceDaily, 6 March 2014.

Photo References

figure 1:

Alzheimer's Brain. Digital image. Pinterest. Sciencephoto, n.d. Web. 29 Apr. 2017.

figure 2:

Pioneering Brain Imaging That Can Detect the Build-up of Destructive Proteins Linked to Alzheimer's Has Been Developed by Japanese Scientists. Digital image. BBC News. N.p., 19 Sept. 2013. Web. 28 Apr. 2017.