Science Current Events | Science News | Brightsurf.com
 
Email a Friend Send to a friend
Printer Friendly Print Enzyme may be a key to Alzheimer's-related cell death

Enzyme may be a key to Alzheimer's-related cell death

October 08, 2009

A Purdue University researcher has discovered that the amount of an enzyme present in neurons can affect the mechanism thought to cause cell death in Alzheimer's disease patients and may have applications for other diseases such as stroke and heart attack.

Sandra Rossie, a professor of biochemistry, found that increasing the amount of protein phosphatase 5, or PP5, in rat neural cells resulted in less cell death associated with reactive oxygen species, which chemically damage cell molecules. Conversely, decreasing PP5 caused greater cell death. The results of Rossie's study are published in the early online version of The Journal of Neurochemistry.




Alzheimer's, a degenerative neurological disease affecting around 5 million people, results in memory loss and dementia. One theory on the cause of Alzheimer's is that overproduction of certain forms of amyloid beta protein by neurons leads to the generation of reactive oxygen species, which activate stress pathways.

"If stress pathways remain active for a prolonged period, the cell will die," Rossie said.

Rossie's lab found that PP5 overexpression prevents neuronal death by amyloid beta and shuts off the stress pathways. When reactive oxygen that wasn't created by amyloid beta was used on the cells, the results were the same. In contrast, neurons with reduced PP5 are more sensitive to death caused by amyloid beta.

"That suggests to us that PP5 protects neurons from cell death induced by reactive oxygen species, not just the presence of amyloid beta," Rossie said. "This means that PP5 may protect against other health problems involving reactive oxygen species as well, such as stroke and heart attacks."

It is possible, Rossie said, that finding a way to increase PP5 activity could help prevent the loss of neurons by amyloid beta.

Rossie said PP5 also could play a role in inhibiting other responses of neurons to amyloid beta. Her lab will work to determine which pathways PP5 affects, and which of those is most responsible for neural protection by PP5.

The National Institutes of Health funded Rossie's research.

Purdue University



Related Amyloid Beta Current Events and Amyloid Beta News Articles Amyloid Beta Current Events and Amyloid Beta News RSS Amyloid Beta Current Events and Amyloid Beta News RSS
Novel mouse gene reduces major pathologies associated with Alzheimer's disease
A new study reveals that a previously undiscovered mouse gene reduces the two major pathological perturbations commonly associated with Alzheimer's disease (AD).

Mouse gene suppresses Alzheimer's plaques and tangles
Investigators at Burnham Institute for Medical Research (Burnham) and colleagues have identified a novel mouse gene (Rps23r1) that reduces the accumulation of two toxic proteins that are major players in Alzheimer's disease: amyloid beta and tau.

Amyloid beta protein gets bum rap
While too much amyloid beta protein in the brain is linked to the development of Alzheimer's disease, not enough of the protein in healthy brains can cause learning problems and forgetfulness, Saint Louis University scientists have found.

Hybrid molecules show promise for exploring, treating Alzheimer's
One of the many mysteries of Alzheimer's disease is how protein-like snippets called amyloid-beta peptides, which clump together to form plaques in the brain, may cause cell death, leading to the disease's devastating symptoms of memory loss and other mental difficulties.

Manipulating Brain Inflammation May Help Clear Brain of Amyloid Plaques, Mayo Clinic Researchers Say
In a surprising reversal of long-standing scientific belief, researchers at the Mayo Clinic campus in Florida have discovered that inflammation in the brain is not the trigger that leads to buildup of amyloid deposits and development of Alzheimer's disease.

Rethinking Alzheimer's disease and its treatment targets
The standard explanation for what causes Alzheimer's is known as the amyloid hypothesis, which posits that the disease results from of an accumulation of the peptide amyloid beta, the toxic protein fragments that deposit in the brain and become the sticky plaques that have defined Alzheimer's for more than 100 years.

Ben-Gurion University Alzheimer's researcher demonstrates specific immune response to vaccine
A researcher who is working on a vaccine for Alzheimer's disease (AD) has demonstrated that it is possible to test and measure specific immune responses in mice carrying human genes and to anticipate the immune response in Alzheimer's patients.

Scientists begin to untangle root cause of Alzheimer's disease
"N60" might not be the first thing that comes to mind when people think of Alzheimer's disease, but thanks to researchers from the United States, South Korea and France, this might change.

Blood flow in Alzheimer's disease
Researchers have discovered that the enzyme, endothelin converting enzyme-2 (ECE-2), may cause the decrease in blood flow in the brain seen in Alzheimer's disease and contribute to progression of the disease.

Vitamin D, curcumin may help clear amyloid plaques found in Alzheimer's disease
UCLA scientists and colleagues from UC Riverside and the Human BioMolecular Research Institute have found that a form of vitamin D, together with a chemical found in turmeric spice called curcumin, may help stimulate the immune system to clear the brain of amyloid beta, which forms the plaques considered the hallmark of Alzheimer's disease.
More Amyloid Beta Current Events and Amyloid Beta News Articles
Alzheimer's Disease: Cellular and Molecular Aspects of Amyloid beta (Subcellular Biochemistry)

Alzheimer's Disease: Cellular and Molecular Aspects of Amyloid beta (Subcellular Biochemistry)
by Robin Harris (Editor), Falk Fahrenholz (Editor)

Preface:

To understand Alzheimer?s disease (AD) is one of the major thrusts of present-day clinical research, strongly supported by more fundamental cellular, biochemical, immunological and structural studies. It is these latter that receive attention within this book. This compilation of 20 chapters indicates the diversity of work currently in progress and summarizes the current state of knowledge. Experienced authors who are scientifically active in their fields of study have been selected as contributors to this book, in an attempt to present a reasonably complete survey of the field. Inevitably, some exciting topics for one reason or another have not been included, for which we can only apologize.

Standardization of terminology is often a problem in science, not least...

[beta]-amyloid Peptide (1-42), Human, Oncogene - Size 250 Ug - Model Pp69--25mg - Each (.25 Mg)

[beta]-amyloid Peptide (1-42), Human, Oncogene - Size 250 Ug - Model Pp69--25mg - Each (.25 Mg)
by Oncogene

[beta]-Amyloid Peptide (1-42), Human, Oncogene - Size 250 ug - Model PP69--25MG - Each (.25 MG) : Lyophilized.Synthetic peptide corresponding to amino acids 1-42 of the processed human amyloid peptide. Supplied in a form that is not neurotoxic prior to preincubation. The level of toxicity has recently been shown to correlate to the extent of beta sheet structure. Reconstitute with degassed HPLC grade deionized water. Purity: >95% by HPLC. FW: 4 kDa.

  Nerve link: Alzheimer's suspect shows up in glaucoma.(This Week)(amyloid beta-protein): An article from: Science News
by N. Seppa (Author)

This digital document is an article from Science News, published by Thomson Gale on August 11, 2007. The length of the article is 483 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available in your Amazon.com Digital Locker immediately after purchase. You can view it with any web browser.

Citation Details
Title: Nerve link: Alzheimer's suspect shows up in glaucoma.(This Week)(amyloid beta-protein)
Author: N. Seppa
Publication: Science News (Magazine/Journal)
Date: August 11, 2007
Publisher: Thomson Gale
Volume: 172 Issue: 6 Page: 84(2)

Distributed by Thomson...

Amyloid Proteins: The Beta Sheet Conformation and Disease

Amyloid Proteins: The Beta Sheet Conformation and Disease
by Jean D. Sipe (Editor)

A first-stop reference on proteins associated with amyloidosis.
This book is the first to present a systematic overview of all known fibril-forming proteins, including their biochemical characteristics and pathophysiology. It considers the clinically recognized amyloid proteins that are known to be associated with the amyloid protein folding disorders, dealing with their common structural and thermodynamic features that lead to amyloid fibril formation and disease. Emphasis is on the thermodynamics of protein folding, the structure and physiologic effects of common oligomeric and subfibrillar intermediates and the influence of the extracellular matrix and cellular trafficking and metabolism on the genesis and catabolism of beta pleated sheet proteins.
The chapters on...

  PET scans show [beta]-Amyloid, promise early Alzheimer's Dx. (Very Preliminary Data).: An article from: Family Practice News
by Miriam E. Tucker (Author)

This digital document is an article from Family Practice News, published by International Medical News Group on September 15, 2002. The length of the article is 468 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available in your Amazon.com Digital Locker immediately after purchase. You can view it with any web browser.

Citation Details
Title: PET scans show [beta]-Amyloid, promise early Alzheimer's Dx. (Very Preliminary Data).
Author: Miriam E. Tucker
Publication: Family Practice News (Magazine/Journal)
Date: September 15, 2002
Publisher: International Medical News Group
Volume: 32 Issue: 18 Page: 2(1)

Distributed by Thomson...

  Beta amyloid: the peptide that kills from both the outside and inside to produce Alzheimer's disease. (Collegiate Communications--Undergraduate).(Brief ... of the North Dakota Academy of Science
by Jason Spah (Author), Katherine Splichal (Author), Kali Wilson (Author), Garl K. Rieke (Author)

This digital document is an article from Proceedings of the North Dakota Academy of Science, published by North Dakota Academy of Science on April 1, 2000. The length of the article is 897 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available in your Amazon.com Digital Locker immediately after purchase. You can view it with any web browser.

Citation Details
Title: Beta amyloid: the peptide that kills from both the outside and inside to produce Alzheimer's disease. (Collegiate Communications--Undergraduate).(Brief Article)
Author: Jason Spah
Publication: Proceedings of the North Dakota Academy of Science (Refereed)
Date: April 1, 2000
Publisher: North Dakota Academy of Science
Page:...

  Brain sabotage: Alzheimer's protein may spawn miniseizures.(This Week)(Amyloid beta-protein): An article from: Science News
by N. Seppa (Author)

This digital document is an article from Science News, published by Thomson Gale on September 15, 2007. The length of the article is 536 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available in your Amazon.com Digital Locker immediately after purchase. You can view it with any web browser.

Citation Details
Title: Brain sabotage: Alzheimer's protein may spawn miniseizures.(This Week)(Amyloid beta-protein)
Author: N. Seppa
Publication: Science News (Magazine/Journal)
Date: September 15, 2007
Publisher: Thomson Gale
Volume: 172 Issue: 11 Page: 165(2)

Distributed by Thomson...

  Genetic variant tied to amyloid-[beta] generation in Alzheimer's.(Geriatric Psychiatry)(Clinical report): An article from: Clinical Psychiatry News
by Jeff Evans (Author)

This digital document is an article from Clinical Psychiatry News, published by Thomson Gale on April 1, 2007. The length of the article is 763 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available in your Amazon.com Digital Locker immediately after purchase. You can view it with any web browser.

Citation Details
Title: Genetic variant tied to amyloid-[beta] generation in Alzheimer's.(Geriatric Psychiatry)(Clinical report)
Author: Jeff Evans
Publication: Clinical Psychiatry News (Magazine/Journal)
Date: April 1, 2007
Publisher: Thomson Gale
Volume: 35 Issue: 4 Page: 25(1)

Article Type: Clinical report

Distributed by Thomson...

  Low plasma [beta]-amyloid levels may be a marker for cognitive decline.(Geriatric Psychiatry): An article from: Clinical Psychiatry News
by Kerri Wachter (Author)

This digital document is an article from Clinical Psychiatry News, published by Thomson Gale on October 1, 2005. The length of the article is 595 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available in your Amazon.com Digital Locker immediately after purchase. You can view it with any web browser.

Citation Details
Title: Low plasma [beta]-amyloid levels may be a marker for cognitive decline.(Geriatric Psychiatry)
Author: Kerri Wachter
Publication: Clinical Psychiatry News (Magazine/Journal)
Date: October 1, 2005
Publisher: Thomson Gale
Volume: 33 Issue: 10 Page: 48(1)

Distributed by Thomson...

  FDG-PET scan targets [beta]-amyloid deposits. (May Predict Alzheimer's).: An article from: Internal Medicine News
by Miriam E. Tucker (Author)

This digital document is an article from Internal Medicine News, published by International Medical News Group on September 1, 2002. The length of the article is 485 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available in your Amazon.com Digital Locker immediately after purchase. You can view it with any web browser.

Citation Details
Title: FDG-PET scan targets [beta]-amyloid deposits. (May Predict Alzheimer's).
Author: Miriam E. Tucker
Publication: Internal Medicine News (Magazine/Journal)
Date: September 1, 2002
Publisher: International Medical News Group
Volume: 35 Issue: 17 Page: 4(1)

Distributed by Thomson...

© 2009 BrightSurf.com