Columbia Science Review
  • Home
  • About
    • Our Team
  • Blog
  • Events
    • 2022-2023
    • 2021-2022
    • 2020-2021
    • 2019-2020
    • 2018-2019
    • 2017-2018
    • 2016-2017
  • Publications
  • COVID-19 Public Hub
    • Interviews >
      • Biology of COVID-19
      • Public Health
      • Technology & Data
    • Frontline Stories >
      • Healthcare Workers
      • Global Health
      • Volunteer Efforts
    • Resources & Links >
      • FAQ's
      • Resource Hubs
      • Student Opportunities
      • Podcasts & Graphics
      • Mental Health Resources
      • Twitter Feeds
      • BLM Resources
    • Columbia Events >
      • Campus Events
      • CUMC COVID-19 Symposium
      • CSR Events
    • Our Team
  • Contact

A Promising Cure for Alzheimer’s Disease?

4/18/2015

0 Comments

 
Picture
By Jack Zhong
Edited By Josephine McGowan

Alzheimer’s disease is the 6th leading cause of death in the US, and yet, it has no known cures, prevention methods, or approaches to slow down the progression of disease. Causing degeneration in the brain, Alzheimer’s disease has common symptoms that include: dementia, memory loss, decline in speech, and confusion. The disease pathology is gradual, with seven major stages. Its victims include former president Ronald Reagan and Nobel laureate physicist Charles Kao, and the disease mainly affects people 65 years and older. Recently, a new drug, Aducanumab (BIIB037), has yielded promising results in clinical trials.

In attempting to treat Alzheimer’s disease and other neurodegenerative disorders, neuroscientists and doctors struggle with a wide gap of knowledge in neuroscience. Neuroscientists understand well how a neuron works on a cellular level, and psychologists have to a certain extent clarified how humans behave. Yet, we do not understand well how the signals of millions of individual neurons throughout the brain integrate together to cause behavior. Similarly, we do not know what goes awry in neural circuitry to cause neurodegenerative diseases, even if we could detect abnormalities in individual neurons. Sometimes, a part of the brain can be removed with little consequence, but a slight mutation in the genes can cause devastating diseases. We simply don’t understand exactly how changes in neurons lead to changes in behavior or brain functions. Given our lack of knowledge in this respect, attempting to treat neurodegenerative diseases is like attempting to treat infectious diseases without knowing how viruses alter organ functions.

Though there are many hypotheses on the causes of Alzheimer’s disease, scientists are still debating what the definitive cause might be. Most of today’s treatments are based on the Cholinergic Hypothesis, which proposes that Alzheimer’s disease is caused by a reduction in acetylcholine, a molecule used in signaling between neurons. However, most drugs used to treat acetylcholine deficiency have not yet been proven to be effective in treating Alzheimer’s. Alternatively, the Amyloid Hypothesis suggests that amyloid beta (Aβ) deposits on the outside of neurons cause the disease. In support of the Amyloid Hypothesis, scientists note that the gene for the amyloid precursor protein (APP) is on chromosome 21, and many Down syndrome patients (with an extra chromosome 21) exhibit Alzheimer’s disease by age 40. Mice with mutated APP genes exhibit amyloid plaques and Alzheimer’s like symptoms. Also, APOE4 is a defective form of a protein that normally breaks down, and people with APOE4 gene are at risk of Alzheimer’s disease. There are still many other hypotheses on the causes of Alzheimer’s disease not mentioned here.

When scientists at the biotech company Neurimmune developed Aducanumab, they sought to tackle the disease based on the Amyloid Hypothesis. Aducanumab is an antibody derived from healthy, aged donors without Alzheimer’s disease. The scientists figured that since the donors’ immune systems were resistant to Alzheimer’s disease, antibodies from these healthy patients could be turned into treatments. This process of turning antibodies from healthy individuals into therapeutics is called "reverse translational medicine."

When determining the mechanism of these antibodies, the scientists found that Aducanumab targets a special recognizable region on the Aβ. Antibodies work by selectively binding to recognizable regions of pathogens called epitopes, and they trigger an immune response to destroy the pathogen. Once in the brain, Aducanumb binds to Aβ that forms aggregates, which is believed to cause Alzheimer’s disease, but the drug leaves single Aβ untouched.

Scientists testing the effectiveness of Aducanumab were greeted with promising results. There are many stages before drugs are released onto the market (Figure 4). Before human testing, scientists dosed mice with mutant APP genes with Aducanumab for thirteen weeks, and all sizes of the Aβ plaques were reduced. After the drug was found to be safe for human use, Biogen Idec started PRIME, a 2012 multi-dose study involving 166 people with Alzheimer’s disease. On March 20, 2015, analysis of the first data was presented. Aducanumab reduced amyloid deposits in 6 regions of the cerebral cortex of the brain. Large effects were observed after 1 year of dosage. The highest dose seems to reduce cortical amyloid close to normal detected levels. Further, cognitive tests administered to patients suggest that Aducanumab reduce cognitive decline in a dose-dependent fashion. PRIME is an ongoing study that will last until 2016.

​The cure for Alzheimer’s disease may be around the corner if Aducanumab continues to yield encouraging results. Regardless of the eventual conclusion on Aducanumab, neuroscientists must continue to hunt down the cause of Alzheimer’s. Most importantly, neuroscientists need to work slowly to close this gap of knowledge in Alzheimer’s on a neuron-level, which can lead to a revolution in our understanding of the brain and treatments of neurological disorders. To achieve this hypothetical goal would mean eventually elucidating the etiology of this disease, as well as finding ways to prevent its progressive damage.
0 Comments



Leave a Reply.

    Categories

    All
    Artificial Intelligence
    Halloween 2022
    Winter 2022-2023

    Archives

    April 2024
    January 2024
    February 2023
    November 2022
    October 2022
    June 2022
    January 2022
    May 2021
    April 2021
    March 2021
    February 2021
    January 2021
    December 2020
    November 2020
    October 2020
    September 2020
    August 2020
    July 2020
    June 2020
    May 2020
    April 2020
    March 2020
    February 2020
    January 2020
    November 2019
    October 2019
    April 2019
    March 2019
    February 2019
    January 2019
    December 2018
    November 2018
    October 2018
    April 2018
    March 2018
    February 2018
    November 2017
    October 2017
    May 2017
    April 2017
    April 2016
    March 2016
    February 2016
    December 2015
    November 2015
    October 2015
    May 2015
    April 2015
    March 2015
    February 2015
    January 2015
    December 2014
    November 2014
    October 2014
    May 2014
    April 2014
    March 2014
    February 2014
    December 2013
    November 2013
    October 2013
    April 2013
    March 2013
    February 2013
    January 2013
    December 2012
    November 2012
    October 2012
    April 2011
    March 2011
    February 2011
    September 2010
    August 2010
    July 2010
    June 2010
    May 2010
    April 2010
    March 2010
    February 2010
    January 2010
    December 2009
    November 2009
    July 2009
    May 2009

Columbia Science Review
© COPYRIGHT 2022. ALL RIGHTS RESERVED.
Photos from driver Photographer, BrevisPhotography, digitalbob8, Rennett Stowe, Kristine Paulus, Tony Webster, CodonAUG, Tony Webster, spurekar, europeanspaceagency, Christoph Scholz, verchmarco, rockindave1, robynmack96, Homedust, The Nutrition Insider
  • Home
  • About
    • Our Team
  • Blog
  • Events
    • 2022-2023
    • 2021-2022
    • 2020-2021
    • 2019-2020
    • 2018-2019
    • 2017-2018
    • 2016-2017
  • Publications
  • COVID-19 Public Hub
    • Interviews >
      • Biology of COVID-19
      • Public Health
      • Technology & Data
    • Frontline Stories >
      • Healthcare Workers
      • Global Health
      • Volunteer Efforts
    • Resources & Links >
      • FAQ's
      • Resource Hubs
      • Student Opportunities
      • Podcasts & Graphics
      • Mental Health Resources
      • Twitter Feeds
      • BLM Resources
    • Columbia Events >
      • Campus Events
      • CUMC COVID-19 Symposium
      • CSR Events
    • Our Team
  • Contact