Monday, November 21, 2011
Clemens Gleich in Die Welt reports on the development of super batteries able to power a smart phone or notebook for days without re-charging. While some researchers try to improve conventional lithium-ion batteries by modifying the carbon-based anode with silicon, others design lithium-oxygen or fluorine-oxygen batteries. Main challenges are safety, prevention of swelling and maintaining a high capacity.
Britta Verlinden in Die Zeit reports on the discovery that dimethyl fumarate, a standard drug used for the treatment of psoriasis since 1994, may also be used as a pill to treat multiple sclerosis. Preliminary results of a Phase III trial demonstrate its ability to significantly reduce the number of attacks. The drug candidate codenamed BG-12 is being developed by Biogen Idec. The paper raises the concern that BG-12 may be sold as MS medication at €15,000 a year – while based on the price of the same compound for psoriasis, costs would amount to €4,400 per year, which already “is clearly more costly than what might be expected based on the cheap basic material”. » Read more...
Tuesday, November 8, 2011
Frankfurter Allgemeine Sonntagszeitung (FAS) this week in a special section (not online yet) deals with prion diseases such as Kuru, Creutzfeldt-Jakob disease, BSE and scrapie and the history of the discovery that some CNS disorders are caused not by pathogens, such as bacteria or viruses, but by infectious proteins. In one of the articles, Volker Stollorz deals with the implication of the discovery. It led to the notion that CNS diseases can be caused by misfolding of proteins, and meanwhile about 2 dozen neurological disorders are classified as “proteopathies”, among them Alzheimer’s disease and Parkinson’s disease. Stollorz features research that points to the possibility that proteopathies spread through the body by some sort of domino effect. In this case, it cannot be ruled out that they are contagious – which would have enormous consequences for medicine. To rule out the possibility that modern medicine contributes to the spread of neurodegenerative diseases, some researchers already call for sterilizing medical instruments with procedures that also deactivate proteins. » Read more...
Tuesday, October 11, 2011
Dieter Durand and Susanne Kutter in Wirtschaftswoche feature a disputation between Alzheimer-researcher Konrad Beyreuther and author Cornelia Stolze, who has written a book claiming Alzheimer’s disease does not exist as an exactly defined disease.
While Beyreuther maintains the disease is real and can be clinically separated from other forms of dementia, he concedes that current medications are useless and that diagnosis often is inadequate. Stolze in her book “Vergiss Alzheimer” (“Forget About Alzheimer’s”) states that patients with signs of dementia often are labeled as Alzheimer’s disease patients although they are not, that they receive useless medications, that the real causes of their respective dementias, such as diabetes, depression, stroke, or dehydration, are overlooked and not treated, and that medical doctors make money with unreliable early diagnostic tests. A review of the book is to follow soon – please regularly check the akampioneer. » Read more...
Monday, September 19, 2011
During the upcoming World Alzheimer Day, the German MDR radio will feature the efforts by German biotechnology company Probiodrug to develop novel strategies for the treatment of Alzheimer’s Disease (AD). MDR’s FIGARO am Vormittag morning magazine will introduce the company’s hypothesis on the onset of Alzheimer’s Disease (AD) and highlight the latest research results published by Probiodrug and co-workers from German and US research institutions in the recent Journal of Neuroscience.
It is well known that the presence of so-called beta-amyloid (A beta) plaques in the brain is not necessarily correlated with the occurrence of AD. Probiodrug discovered that in AD patients, the core of the plaques is made form a certain variant of the A beta peptide which is more neurotoxic, less soluble and able to rapidly aggregate with modified and unmodified A beta. Further investigations revealed that this toxic variant is generated by an enzyme called QC (glutaminyl cyclase). QC is responsible for activating certain hormones and enzymes in the brain by modifying a certain chemical group in these molecules. If it starts acting on A beta, it produces the toxic variant. Probiodrug also has demonstrated in various experiments that it is possible to prevent the formation or spread of toxic A beta plaques by switching off the QC enzyme. The company therefore is developing drugs to inhibit the enzyme as a potential treatment strategy to either prevent the onset of AD or slow down the progression of the disease. » Read more...
Thursday, September 8, 2011
Probiodrug provides further insights into the onset of AD in The Journal of Neuroscience
Probiodrug AG (Probiodrug), a biotech company developing novel products for the treatment of neurodegenerative and inflammatory disorders, today announced the publication of data providing key insights into the onset and development of Alzheimer’s disease (AD) in the Journal of Neuroscience (http://redir.ec/jneurosci).
AD is characterized by deposition of amyloid-β (Aβ) plaques in the brain. However, quantitative relationship between plaque deposition and severity of cognitive decline in the affected individuals is still elusive. Often, elderly people carry a large amyloid burden without any signs of cognitive impairments, and many animal models of AD also develop the characteristic hallmarks, such as plaques, but do not demonstrate the cognitive defects and loss of neurons typical of the human disease.
Several years ago, Probiodrug developed the hypothesis that the missing link between Aβ load and prevalence of AD is a certain modification of Aβ, in which the Aβ molecule carries a pyroglutamate residue (pGlu) at its N-terminus. This pGlu-Aβ is neurotoxic and develops a strong tendency to aggregate and to seed aggregation of further pGlu-Aβ as well as unmodified Aβ. The modification of glutamic acid to a pGlu-residue is catalyzed by the so-called QC enzyme (glutaminyl cyclase). » Read more...