• HOME
  • NEWS
  • EXPLORE
    • CAREER
      • Companies
      • Jobs
    • EVENTS
    • iGEM
      • News
      • Team
    • PHOTOS
    • VIDEO
    • WIKI
  • BLOG
  • COMMUNITY
    • FACEBOOK
    • INSTAGRAM
    • TWITTER
Saturday, August 2, 2025
BIOENGINEER.ORG
No Result
View All Result
  • Login
  • HOME
  • NEWS
  • EXPLORE
    • CAREER
      • Companies
      • Jobs
        • Lecturer
        • PhD Studentship
        • Postdoc
        • Research Assistant
    • EVENTS
    • iGEM
      • News
      • Team
    • PHOTOS
    • VIDEO
    • WIKI
  • BLOG
  • COMMUNITY
    • FACEBOOK
    • INSTAGRAM
    • TWITTER
  • HOME
  • NEWS
  • EXPLORE
    • CAREER
      • Companies
      • Jobs
        • Lecturer
        • PhD Studentship
        • Postdoc
        • Research Assistant
    • EVENTS
    • iGEM
      • News
      • Team
    • PHOTOS
    • VIDEO
    • WIKI
  • BLOG
  • COMMUNITY
    • FACEBOOK
    • INSTAGRAM
    • TWITTER
No Result
View All Result
Bioengineer.org
No Result
View All Result
Home NEWS Science News Biology

Cause of Alzheimer’s disease traced to mutation in common enzyme

Bioengineer by Bioengineer
October 24, 2020
in Biology
Reading Time: 3 mins read
0
Share on FacebookShare on TwitterShare on LinkedinShare on RedditShare on Telegram

Mutation to MARK4 makes proteins stickier and more likely to clump in brain

IMAGE

Credit: Tokyo Metropolitan University

Tokyo, Japan – Researchers from Tokyo Metropolitan University have discovered a new mechanism by which clumps of tau protein are created in the brain, killing brain cells and causing Alzheimer’s disease. A specific mutation to an enzyme called MARK4 changed the properties of tau, usually an important part of the skeletal structure of cells, making it more likely to aggregate, and more insoluble. Getting to grips with mechanisms like this may lead to breakthrough treatments.

Alzheimer’s disease is a life-changing, debilitating condition, affecting tens of millions of people worldwide. According to the World Health Organization, it is the most common cause of senile dementia, with numbers worldwide expected to double every 20 years if left unchecked.

Alzheimer’s is said to be caused by the build-up of tangled clumps of a protein called “tau” in brain cells. These sticky aggregates cause neurons to die, leading to impairment in memory and motor functions. It is not yet clear how and why tau builds up in the brain cells of Alzheimer’s patients. Understanding the cause and mechanism behind this unwanted clumping would open up the way to new treatments and ways to prevent the disease.

A team led by Associate Professor Kanae Ando of Tokyo Metropolitan University has been exploring the role played by the MARK4 (Microtubule Affinity Regulating Kinase 4) enzyme in Alzheimer’s disease. When everything is working normally, the tau protein is an important part of the structure of cells, or the cytoskeleton. To keep the arms of the cytoskeleton or microtubules constantly building and disassembling, MARK4 actually helps tau detach from the arms of this structure.

Problems start when a mutation occurs in the gene that provides the blueprint for making MARK4. Previous work had already associated this with an increased risk of Alzheimer’s, but it was not known why this was the case. The team artificially introduced mutations into transgenic drosophila fruit flies that also produce human tau, and studied how the proteins changed in vivo. They discovered that this mutant form of MARK4 makes changes to the tau protein, creating a pathological form of tau. Not only did this “bad” tau have an excess of certain chemical groups that caused it to misfold, they found that it aggregated much more easily and were no longer soluble in detergents. This made it easier for tau to form the tangled clumps that causes neurons to degenerate.

MARK4 has also been found to cause a wide range of other diseases which involve the aggregation and buildup of other proteins. That’s why the team’s insights into tau protein buildup may lead to new treatments and preventative measures for an even wider variety of neurodegenerative conditions.

###

This work was supported by a Grant-in-Aid for Scientific Research on Innovative Areas (Brain Protein Aging and Dementia Control) [JSPS KAKENHI Grant number 17H05703], a research award from the Hoan-sha Foundation, the Takeda Science Foundation, a research award from the Japan Foundation for Aging and Health, a Grant-in-Aid for Scientific Research on Challenging Research (Exploratory) [JSPS KAKENHI Grant number 19K21593], and Research Funding for Longevity Science 19-7 from the National Center for Geriatrics and Gerontology, Japan.

Media Contact
Go Totsukawa
[email protected]

Related Journal Article

http://dx.doi.org/10.1074/jbc.RA120.014420

Tags: AlzheimerBiochemistryBiologyCell BiologyMolecular BiologyneurobiologyNeurochemistry
Share14Tweet9Share2ShareShareShare2

Related Posts

blank

CK2–PRC2 Signal Drives Plant Cold Memory Epigenetics

August 2, 2025
blank

AI-Driven Protein Design Advances T-Cell Immunotherapy Breakthroughs

August 1, 2025

Melanthiaceae Genomes Reveal Giant Genome Evolution Secrets

August 1, 2025

“Shore Wars: New Study Tackles Oyster-Mangrove Conflicts to Boost Coastal Restoration”

August 1, 2025
Please login to join discussion

POPULAR NEWS

  • Blind to the Burn

    Overlooked Dangers: Debunking Common Myths About Skin Cancer Risk in the U.S.

    60 shares
    Share 24 Tweet 15
  • Neuropsychiatric Risks Linked to COVID-19 Revealed

    42 shares
    Share 17 Tweet 11
  • Dr. Miriam Merad Honored with French Knighthood for Groundbreaking Contributions to Science and Medicine

    46 shares
    Share 18 Tweet 12
  • Study Reveals Beta-HPV Directly Causes Skin Cancer in Immunocompromised Individuals

    38 shares
    Share 15 Tweet 10

About

We bring you the latest biotechnology news from best research centers and universities around the world. Check our website.

Follow us

Recent News

Magnesium Implants Boost Bone-Immune Health In Vitro

Unmet Supportive Care Needs in Cancer Patients

AI Virtual Lab Engineers New SARS-CoV-2 Nanobodies

  • Contact Us

Bioengineer.org © Copyright 2023 All Rights Reserved.

Welcome Back!

Login to your account below

Forgotten Password?

Retrieve your password

Please enter your username or email address to reset your password.

Log In
No Result
View All Result
  • Homepages
    • Home Page 1
    • Home Page 2
  • News
  • National
  • Business
  • Health
  • Lifestyle
  • Science

Bioengineer.org © Copyright 2023 All Rights Reserved.