Features | Partner Sites | Information | LinkXpress
Sign In
GLOBETECH MEDIA
GLOBETECH PUBLISHING LLC
GLOBETECH PUBLISHING LLC

Blocking Alzheimer’s Disease Process by Blocking Specific Protein

By BiotechDaily International staff writers
Posted on 13 May 2013
Scientists have discovered a potential approach for developing treatments to stop the disease process in Alzheimer’s disease (AD). The strategy is based on unclogging and removing the toxic debris that gathers in patients’ brains, by suppressing activity of a little-known regulator protein called CD33.

“Too much CD33 appears to promote late-onset Alzheimer’s by preventing support cells from clearing out toxic plaques, key risk factors for the disease,” explained Rudolph Tanzi, PhD, of Massachusetts General Hospital (Boston, MA, USA) and Harvard University (Cambridge, MA, USA), a grantee of the US National Institutes of Health’s (NIH; Bethesda, MD, USA) National Institute of Mental Health (NIMH) and National Institute on Aging (NIA).“Future medications that impede CD33 activity in the brain might help prevent or treat the disorder.”

Dr. Tanzi and colleagues reported their findings April 25, 2013, in the journal Neuron. Variation in the CD33 gene appeared as one of four prime suspects in the largest genome-wide dragnet of Alzheimer's-affected families, reported by Dr. Tanzi and colleagues in 2008. The gene was known to make a protein that controls the immune system, but its function in the brain remained elusive. To find out how it might contribute to AD, the researchers conducted human genetics, biochemistry, and human brain tissue, mouse, and cell-based research.

The scientists found over-expression of CD33 in support cells, called microglia, in postmortem brains from patients who had late-onset AD, the most typical form of the disorder. The more CD33 protein on the cell surface of microglia, the more beta-amyloid proteins and plaques had accumulated in their brains. Moreover, the researchers discovered that brains of people who inherited a version of the CD33 gene that protected them from AD noticeably exhibited reduced amounts of CD33 on the surface of microglia and less beta-amyloid.

Brain levels of beta-amyloid and plaques were also significantly decreased in mice modified to under-express or lack CD33. Microglia cells in these animals were more effective at clearing out the debris, which the researchers tracked to levels of CD33 on the cell surface.

New findings also suggested that CD33 works in league with another AD risk gene in microglia to regulate inflammation in the brain. The study’s findings, as well as those of a recent lab rodent study that replicated numerous characteristics of the human disorder, add support to the prevailing theory that accumulation of beta-amyloid plaques are hallmarks of Alzheimer’s pathology. They come at a time of upheaval in the field, triggered by other recent contradictory findings suggesting that these reputed offenders might instead play a protective role.

Because increased CD33 activity in microglia impaired beta-amyloid clearance in late onset AD, Dr. Tanzi and colleagues are now searching for agents that can cross the blood-brain barrier and block it.

Related Links:

Massachusetts General Hospital
National Institute of Mental Health



Channels

Genomics/Proteomics

view channel
Image: Transmission electron micrograph of norovirus particles in feces (Photo courtesy of Wikimedia Commons).

Norovirus Interacts with Gut Bacteria to Establish a Persistent Infection That Can Be Blocked by Interferon Lambda

A team of molecular microbiologists and virologists has found that norovirus requires an intimate interaction with certain gut bacteria to establish a persistent infection, and that the infective process... Read more

Biochemistry

view channel

Possible New Target Found for Treating Brain Inflammation

Scientists have identified an enzyme that produces a class of inflammatory lipid molecules in the brain. Abnormally high levels of these molecules appear to cause a rare inherited eurodegenerative disorder, and that disorder now may be treatable if researchers can develop suitable drug candidates that suppress this enzyme.... Read more

Therapeutics

view channel
Image: Cancer cells infected with tumor-targeted oncolytic virus (red). Green indicates alpha-tubulin, a cell skeleton protein. Blue is DNA in the cancer cell nuclei (Photo courtesy of Dr. Rathi Gangeswaran, Bart’s Cancer Institute).

Innovative “Viro-Immunotherapy” Designed to Kill Breast Cancer Cells

A leading scientist has devised a new treatment that employs viruses to kill breast cancer cells. The research could lead to a promising “viro-immunotherapy” for patients with triple-negative breast cancer,... Read more

Lab Technologies

view channel
Image: MIT researchers have designed a microfluidic device that allows them to precisely trap pairs of cells (one red, one green) and observe how they interact over time (Photo courtesy of Burak Dura, MIT).

New Device Designed to See Communication between Immune Cells

The immune system is a complicated network of many different cells working together to defend against invaders. Effectively combating an infection depends on the interactions between these cells.... Read more

Business

view channel

Program Designed to Provide High-Performance Computing Cluster Systems for Bioinformatics Research

Dedicated Computing (Waukesha, WI, USA), a global technology company, reported that it will be participating in the Intel Cluster Ready program to deliver integrated high-performance computing cluster solutions to the life sciences market. Powered by Intel Xeon processors, Dedicated Computing is providing a range of... Read more
 
Copyright © 2000-2015 Globetech Media. All rights reserved.