Food for Thought: “Forget Alzheimer’s”? – A Book Review


Thursday, February 2, 2012

“Forget Alzheimer’s” is the title and the message of a book by German journalist Cornelia Stolze who is claiming to tell the “truth about a disease which isn’t one” (Cornelia Stolze, Vergiss Alzheimer. Die Wahrheit über eine Krankheit, die keine ist, Köln/Cologne 2011: Kiepenheuer & Witsch).

The book is strongly criticizing the handling of dementia, in particular Alzheimer’s disease (AD) in today’s medicine, pointing out the lack of adequate diagnostics and therapies and contrasting this sad reality with the often exaggerated promises of imminent breakthroughs by experts.

Stolze starts by explaining that to date, it is extremely difficult to diagnose Alzheimer’s disease. Most claims about new methods to confirm a diagnosis or, even better, to predict the onset have turned out to be false. She also points out that about 50 diseases and at least 150 medications may cause dementia symptoms. She concludes that most physicians are overextended to differentiate and often too early and too easily put the patient down as having Alzheimer’s, thereby impeding a causal treatment and condemning the patient to unnecessary mental derangement.

Company News: Probiodrug’s Hypothesis on Alzheimer’s Disease Onset Featured in German Radio


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.

Company News: Neurodegeneration in Alzheimer’s Disease: The crucial role of QC


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).

Food for Thought: Weekly Wrap-Up


Monday, March 14, 2011

Joachim Müller-Jung in Frankfurter Allgemeines Zeitung (FAZ) this week deals with the ethic implications of non-invasive prenatal diagnosis, describing that a huge number of tests based on fetal DNA entering the mother’s blood stream is ready to enter the market. His recommendation is to start an immediate discussion about which tests should be applied and which ones should not.

Ulrich Bahnsen in Die ZEIT interviews Norbert Donner-Banzhoff, Professor at the University of Marburg’s Department of General Practice, Preventive and Rehabilitative Medicine. Donner-Banzhoff conducted a study published in the Canadian Medical Association Journal CMAJ investigating the influence of pharmaceutical advertising on the drug recommendations made in articles in 11 German journals that focus on medical education. Donner-Banzhoff and his team come to the conclusion that journals financed by advertisement from the pharma industry and given away for free almost exclusively recommended the use of specified drugs, whereas journals financed entirely with subscription fees tended to recommend against the use of the same drugs. In the interview, Donner-Banzhoff suggests that a lot of articles published in the free journals have been written by ghost writers and/or members of the pharmaceutical industry.

Food for Thought: Probiodrug’s Alzheimer Hypothesis Independently Confirmed


Thursday, March 10, 2011

Two decades ago, it was discovered by the founders of German biotech company Probiodrug that the so-called amyloid beta peptides (Aβ) forming the notorious plaques in the brain of Alzheimer’s Disease (AD) patients are not a homogeneous species. While it was known that there are variants in length (from 36 to 43 amino acids), the Probiodrug researchers discovered that there also are pyroglutamated variants (pGlu-Aβ) of the peptides. However, little was known about their origin and biological role. This has changed significantly over the last years, and Probiodrug has pioneered this research.

At this year’s 10th International Conference on Alzheimer’s and Parkinson’s Diseases (AD/PD 2011), taking place in Barcelona/Spain from March 9 to 13, more than two dozen posters and presentations provide further insights into the mechanisms and consequences of pGlu-Aβ formation, and there is overwhelming evidence that pGlu-Aβ is key to understanding Alzheimer’s Disease and to developing novel treatments. Abstracts can be found here.

The findings can be summarized as follows:

1.    Amyloid plaques alone correlate poorly with the severity of AD.

2.    The presence of pGluAβ in plaques, however, does correlate with disease severity in both sporadic and familial AD.