Apolipoprotein D protects against Alzheimer’s



Sunesis Pharmaceuticals, Inc. presented data from three clinical trials of the company’s lead drug candidate, voreloxin (formerly SNS-595), at the Chemotherapy Foundation Symposium held in New York on November 4-8. Data previously presented from Phase 1 and Phase 1b/2 studies in patients with acute myeloid leukemia (AML) showed that preliminary clinical responses were observed in

Full Post: Sunesis Pharmaceuticals presents data of Voreloxin in patients with acute myeloid leukemia and ovarian cancer

Research on the mechanisms involved in neurodegenerative diseases such as Alzheimer’s, stroke, dementia, Parkinson’s and multiple sclerosis, to name a few, has taken a step forward thanks to the work of biological sciences Ph.D. student Sonia Do Carmo, supervised by Professor ?ic Rassart of the Université du Québec ?ontreal (UQAM) Biological Sciences Department, in collaboration with researchers at the Armand-Frappier Institute and the University of Valladolid in Spain.

Do Carmo and her collaborators have successfully demonstrated the protective and reparative role of apolipoprotein D, or ApoD, in neurodegenerative diseases. Their discovery suggests interesting avenues for preventing and slowing the progression of this type of illness.

These studies were inspired by work done ten years ago by Professor Rassart’s team, who then discovered increased levels of ApoD in the brains of people with several types of neurodegenerative disorders, including Alzheimer’s. The team hypothesized that this protein might play a protective and restorative role but were unable to demonstrate this at the time.

The experiments

To establish the protective and reparative role of ApoD, the researchers used two types of genetically modified mice: one type with increased levels of ApoD in the brain and a second type with no ApoD. The mice were then exposed to neurodegenerative agents. A group of the modified mice and a control group (unmodified) were exposed to paraquat, a widely used herbicide that has been shown to increase the risk of Parkinson’s. Then the same type of experiment was performed by injecting two groups with a virus that causes encephalitis. In both cases, the mice modified for increased levels of ApoD had the best outcomes, with a better ability to combat the diseases and a higher survival rate than the unmodified mice. The knockout mice with no ApoD displayed the poorest outcomes. These experiments serve to illustrate the protective and reparative role of this protein.

When can we expect medication?

A number of steps remain before this research can translate into effective drugs against neurodegenerative conditions. The original investigator, Professor ?ic Rassart, explains, “You cannot simply inject ApoD, as it has to enter the brain in order for it to be active. We have successfully demonstrated the role of ApoD, but now we need to understand the action of this protein. Only then will we be able to think about creating a drug to prevent these types of diseases and to slow their progression. All the same, this discovery by Sonia Do Carmo and her collaborators is a significant breakthrough, as we know very little about the mechanisms of neurodegenerative diseases.”

The discovery has aroused considerable interest among the molecular biology community. Two major scientific journals have already published the research findings: Aging Cell (Vol. 7: 506-515, 2008) and Journal of Neuroscience (Vol. 28: 10330-10338, 2008).

http://www.uqam.ca/

Link




Neurologists have observed for decades that Lewy bodies, clumps of aggregated proteins inside cells, appear in the brains of patients with Parkinson’s disease and other neurodegenerative diseases. The presence of Lewy bodies suggests underlying problems in protein recycling and waste disposal, leading to the puzzle: how does disrupting those processes kill brain cells? One possible

Full Post: Discovery of potential important pathway for controlling cell loss and survival in Parkinson’s disease



Australian scientists at CSIRO (Commonwealth Scientific and Industrial Research Organisation), have developed a new system to screen for compounds that can inhibit one of the processes that takes place during the progression of Alzheimer’s disease. In a paper published in the November issue of the Journal of Alzheimer’s Disease, folate is shown to be beneficial

Full Post: Breakthrough in Alzheimer’s disease screening



For the first time researchers have shown that a commonly used anesthetic can produce changes associated with Alzheimer’s disease in the brains of living mammals, confirming previous laboratory studies. In their Annals of Neurology report, which has received early online release, a team of Massachusetts General Hospital (MGH) investigators shows how administration of the gas

Full Post: Isoflurane induces Alzheimer’s-associated changes in mouse brains



Prana Biotechnology has announced that a recent independent study conducted by Massachusetts General Hospital (MGH) has demonstrated that the Company’s Metal-Protein Attenuating Compounds (MPACs) could halt Alzheimer’s pathology. The study published in the November edition of Annals of Neurology shows that the administration of the anesthetic gas isoflurane can spur the production of amyloid-beta protein,

Full Post: Prana Biotechnology’s compound could halt Alzheimer’s pathology



Recent animal studies have shown that clioquinol - an 80-year old drug once used to treat diarrhea and other gastrointestinal disorders - can reverse the progression of Alzheimer’s, Parkinson’s and Huntington’s diseases. Scientists, however, had a variety of theories to attempt to explain how a single compound could have such similar effects on three unrelated

Full Post: Clioquinol - gastrointestinal drug could become anti-aging treatment