Citrus fruit and carrots protect against Alzheimer’s disease, a press release recently published by the University of Ulm suggests. A closer look at the language used though reveals the statement to be rather hypothetical. However, accuracy does not seem to be a concern of articles aimed at the general public, and this is exactly how expectations and hype are created. The neurologist Christine von Arnim now faces the - not inconsiderable - task of having to scale down expectations and put the Ulm researchers’ work into its correct context.
Boehringer Ingelheim and Vitae Pharmaceuticals Inc. announced today that they have entered into a significant worldwide collaboration to research and develop beta-secretase BACE inhibitors for the treatment of Alzheimers disease.
A study carried out by an international team of scientists, including scientists from the Freiburg University Medical Centre, pooled 16,000 probands and produced large datasets for the identification of genes with an elevated risk for Alzheimer’s disease.
Pathological protein deposits linked to Alzheimers disease and cerebral amyloid angiopathy can be triggered not only by the administration of pathogenic misfolded protein fragments directly into the brain but also by peripheral administration outside the brain. This is shown in a new study done by researchers at the Hertie Institute of Clinical Brain Research in Tübingen.
Prions are misfolded proteins that are associated with diseases such as BSE, Creutzfeldt-Jakob disease and scrapie. What makes prions particularly dangerous is their ability to induce properly folded proteins to convert into misfolded prion forms. This principle seems to be more widespread than previously thought. Dr. Mathias Jucker from the University of Tübingen and his American colleague Lary Walker from Emory University have put forward a hypothesis according to which neurodegenerative diseases such as Alzheimer’s are – similarly to prions - caused by misfolded proteins that aggregate into harmful seeds.
A team at the Hertie Institute for Clinical Brain Research at the University of Tübingen, in cooperation with an international team of scientists, has developed a new transgenic mouse model for Alzheimer’s disease that led to an unexpected result: microglia are not involved in either the formation or the clearance of amyloid plaques.
A large multicentre study has shown that CSF (cerebrospinal fluid) biomarkers can be used to predict, with good accuracy, as to which patients with mild cognitive impairments will develop Alzheimer’s disease. The biomarkers used are microtubule-associated proteins that are abundant in CNS neurons as well as beta amyloid, which is a peptide that forms brain plaques in people with Alzheimer’s disease. Changes in the concentrations of these proteins can be used to identify incipient AD.
The initial consensus guidelines for the postmortem diagnosis of Alzheimer’s disease were published in 1997. In the same year, Dietmar Thal started his four-year research project at the Institute of Anatomy at the University of Frankfurt under the supervision of Heiko Braak, who was then one of the leading figures in Alzheimer’s research, notably for his achievements in grading the presence and distribution of tau tangles in the brain in 1991. In 2012, Dietmar Thal took up where Braak had left off and became a member of the group of experts tasked with updating the 1997 guidelines.
105 years after the first description of the Alzheimers disease by the German neuropsychiatrist Alois Alzheimer the disease still remains a mystery. Around 25000 researchers worldwide are focusing on Alzheimers and are coming up with a broad range of theories and hypotheses on its pathogenesis and potential therapies.
Neurons are very sensitive to disturbances and many different functions are no longer able to work efficiently when the power supply is impaired. Prof. Dr. Chris Meisinger and his team at the Institute of Biochemistry and Molecular Biology at the University of Freiburg have found that amyloid-beta peptides block important enzymes in the mitochondria resulting in mitochondrial dysfunction.
The combination of a newly developed bioinformatic model and experimental data provides new insights into the causes of Alzheimers disease. Researchers found that whilst the activity of a particular enzyme is reduced specific nerve cells are able to counteract this deficiency by rerouting the metabolic fluxes.
The German Research Foundation (DFG) is to fund an interdisciplinary group of researchers led by scientists from Heidelberg. The Transregio research group deals with the physiological functions of the APP gene family that plays an essential role in the pathogenesis of Alzheimer’s (AD). AD is one of the themes at “Neurowoche 2010”, the largest clinical neurosciences congress in Europe, which will be held in Mannheim.
Alzheimers disease is characterised by changes in the substance and structure of the brain that are caused by the depositing of protein plaques in the brain. Prof. Michael Przybylski and his team of researchers at the University of Constance have deciphered the structure of the site where mouse antibodies attach to the plaques subsequently causing them to dissolve. These findings will now be used to identify the binding structure of a component of the human bodys immune defence that counteracts these deposits and to develop a selective vaccine.
On July the 22nd of 2009, the European Commission adopted concrete proposals to tackle Alzheimer’s disease, dementias and other neurodegenerative conditions. These shared health and social challenges in Europe call for coordinated actions to ensure efficient prevention, diagnosis, treatment and care for those affected.
The first lapses of memory go hand in hand with a loss of the sense of smell: The olfactory centre in the brain of Alzheimer’s patients is wasting away. The olfactory bulb starts to shrink at a very early stage of the disease, at a time when retentiveness is only slightly affected. It is possible to detect the shrinkage of the olfactory bulb with magnetic resonance imaging, as the latest findings by scientists of the Department of Psychiatry at the University Hospital of Heidelberg have revealed. The study of the new diagnostic marker was published in May 2009 in the “Journal of Alzheimer’s Disease”.
Researchers believe that the defective transport of proteins can be linked with diseases such as Alzheimer’s. Prof. Dr. Elke Deuerling and Dr. Martin Gamerdinger, molecular biologists from the University of Konstanz, have now discovered what is necessary to prevent erroneous protein transport.
Amyloid fibrils consisting of clumped α-synuclein protein are characteristic of Parkinson's disease. Chaperones, which ensure the correct folding of newly synthesised polypeptides, can inhibit α-synuclein aggregation and, as a consequence, prevent fibrils from forming. Researchers from Heidelberg have shown that a specific combination of human molecular chaperones is able to disassemble fibrils and transform them into non-toxic α-synuclein monomers.
The controlled transport of calcium across cell membranes is crucial for many biological processes including the transfer of information into the brain kidney function and the rhythmic activity of the heart muscle. A team led by Prof. Dr. Norbert Klugbauer at the University of Freiburg is focused on elucidating the function of calcium channels the proteins that regulate them and the effects on learning and memory. The researchers are investigating the molecular mechanisms and electrical properties of calcium channels as well as using mice to gain insights into calcium-dependent memory. At the moment they are concentrating on a calcium channel that was discovered in plants.
“Memory is one of the most exciting research topics I know because it is so close to human reality”, says Christine von Arnim. The Alzheimer’s disease researcher from the University of Ulm is not the only researcher who is intrigued by the philosophy behind the research and interested in far more than just atomistic approaches. The young neurologist covers the entire field of Alzheimer’s research, from experimental laboratory research to patient treatment and care.
Andrei Sommer from the University of Ulm and colleagues from Ulm, Heidelberg and Berlin have succeeded in reducing amyloid beta deposits in human neuroblastoma cells by up to 60 per cent in vitro. The researchers found that the apparently strange combination of green tea and red light has the potential to lead to the development of new therapies for Alzheimer’s. There are currently no treatments available that stop or reverse the progression of the disease.
Scientists from the Hertie Institute for Clinical Brain Research at the University of Tübingen are pursuing an innovative treatment approach for Alzheimer’s disease using immune cells to eliminate the protein deposits that are the hallmark of Alzheimer’s. Dr. Jonas Neher and his team tested whether exchanging brain-specific immune cells with fresh, more active cells has a positive effect on the disease.
It starts with memory loss and disorientation. Alzheimer’s disease is the most common type of dementia and is characterised by the loss of neurons and synapses in the brain resulting from the aggregation of beta amyloid protein fragments into fibrils and plaques. Prof. Dr. Knut Biber and his team from the Division of Molecular Psychiatry at Freiburg University Medical Center have analysed these plaques in an in vivo-like cell culture system. They found that microglial cells can prevent the formation of beta amyloid plaques for quite a long period of time but eventually lose the ability to do so.
The BioMed X Innovation Center and the biopharmaceutical company AbbVie Deutschland GmbH & Co. KG have used crowdsourcing to set up a team of scientists from renowned international institutions to investigate new options for treating Alzheimer’s disease. The team are looking for targets in the metabolism of tau proteins and its pathological modifications that can be used to develop drugs to treat Alzheimer’s disease.
Turmeric: Indians swear by the use of this yellow spice and believe in its healing power. In India, turmeric (curcumin) is believed to protect against cancer and help reduce the incidence of Alzheimer’s disease. Along with four academic and five industrial partners, Dr. Jan Frank from the University of Hohenheim is investigating how the effect of curcumin can be enhanced. The German Ministry of Education and Research is supporting the consortium with funds totalling 1.5 million euros, of which 462,000 euros are allocated to the Hohenheim researchers, giving the project the status of a “heavyweight” research area at the University of Hohenheim.
Neuroscientists from Heidelberg have created the scientific foundations for a nasal spray that can stabilise the dendrites of nerve cells, thus reducing nerve damage and brain function losses following a stroke. Prof. Dr. Hilmar Bading and his team received the 2016 German BioRegions Innovation Prize for their invention and have set up a company called FundaMental Pharma to further accelerate the development of a marketable medicinal product.