The Study

Researchers led by Prof. Graessel, from Friedrich-Alexander-University Erlangen, included in their study patients with dementia from five nursing homes in Bavaria. After random selection, half the patients were included on the year-long MAKS ‘intervention’ consisting of two hours of group therapy, six days a week. In addition all patients maintained their normal treatment and regular activities provided by the nursing home.

The MAKS system consists of motor stimulation(M), including games such as bowling, croquet, and balancing exercises; cognitive stimulation (K), in the form of individual and group puzzles; and practicing ‘daily living’ activities (A), including preparing snacks, gardening and crafts. The therapy session began with a ten minute introduction, which the researchers termed a ‘spiritual element’ (S), where the participants discussed topics like ‘happiness’, or sang a song or hymn.

After 12 months of therapy the MAKS group maintained their level on the Alzheimer’s Disease Assessment Scale (ADAS) and, even more importantly maintained their ability to carry out activities of daily living, while the control group all showed a decrease in cognitive and functional ability.

Prof. Graessel explained, “While we observed a better result for patients with mild to moderate dementia, the result of MAKS therapy on ADAS (cognitive function) was at least as good as treatment with cholinesterase inhibitors. Additionally we found that the effect on the patients’ ability to perform daily living tasks (as measured by the Erlanger Test of Daily Living (E-ADL)) was twice as high as achieved by medication. This means that MAKS therapy is able to extend the quality of, and participation in, life for people with dementia within a nursing home environment. We are currently in the process of extending these preliminary results to see if this prevention of dementia decline can be maintained over a longer time period.”

Full bibliographic information Non-pharmacological, multicomponent group therapy in patients with degenerative dementia: a 12-month randomised, controlled trial, Elmar Graessel, Renate Stemmer, Birgit Eichenseer, Sabine Pickel, Carolin Donath, Johannes Kornhuber and Katharina Luttenberger, BMC Medicine (in press).

Technorati Tags: Balance Exercises, cholinesterase inhibitors, cognitive function, Dementia, Motor Exercises

Technorati Tags: aging, Brain Damage, curcumin, demential, traumatic brain injury

From the Wall Street Journal

By SHIRLEY S. WANG

The hunt for a substance that can improve memory took a promising turn Wednesday, as researchers said they had found a method that appears to reduce forgetting in rats.

According to a study published in the journal Nature, scientists from Mount Sinai School of Medicine in New York showed for the first time that a molecule that occurs naturally in the human brain during memory formation appeared to help rats enhance the strength and duration of some types of memories.

Researchers said that when the substance—known as IGF-II, a protein-like molecule important for cell growth and development as well as tissue repair—was blocked from the brain, the rats didn’t remember what they had learned.

The findings are notable in part because they showed improvement in an area of memory known as declarative memory—the ability to remember places, facts and things. Declarative memory is affected in Alzheimer’s disease and other forms of dementia, and researchers have long sought ways to improve or preserve it.

It is too early to say whether IGF-II will be useful in humans, but the substance may hold more promise than molecules that have been studied up to now, according to Elizabeth Phelps, a cognitive neuroscientist at New York University who studies human learning and memory. Dr. Phelps, who wasn’t involved in the study, called the Nature research “rigorous” and thoroughly conducted.

One advantage of IGF-II is that it can cross the blood-brain barrier, so it could potentially be administered through the bloodstream or as a vapor through the nose, rather than injected directly into the brain. And because it exists in the body already, it’s unlikely to be toxic.

However, researchers will watch for unwanted effects on other cells in the body, said Cristina Alberini, a neuroscience professor at Mount Sinai and the senior author of the paper.

Certain proteins and molecules are needed to build and strengthen connections between nerve cells in the brain to form new long-term memories, and IGF-II appears to be one of those molecules. But more research is needed, according to Dr. Alberini.

“The more we know, the more we’re going to uncover what are the steps that make memory strong,” she said. “Then we’ll get ideas for other [molecular] targets.”

In the study, the rats were placed in a two-compartment cage where they would receive a mild foot shock at one end. They quickly learned to avoid that area. Some rats were then given an injection of IGF-II, in a part of their brain called the hippocampus. Even weeks later, rats that had received the IGF-II exhibited greater avoidance of the location than rats that had a control injection of another growth factor or saline solution.

The effect was seen only in certain parts of the brain. IGF-II didn’t appear to improve memory in the amygdala, which deals more with memories of emotional reactions like fear.

The next step is to administer IGF-II to the entire body to see if it can produce the same memory-boosting effects as direct injection into brain regions, Dr. Alberini said.

Technorati Tags: IGF-II, insulin growth factor II

To fulfill their different functions, proteins have to acquire the correct three-dimensional structure. In other words, polypeptides have to fold first. Molecular chaperones, a diverse group of conserved proteins, have specialized to assist other proteins during their folding. If the chaperones fail, misfolding and aggregation of the newly synthesized and pre-existing proteins might occur. In the worst case, this results then in neurodegenerative diseases, such as Alzheimer’s, Huntington’s chorea or Parkinson’s. Alzheimer’s disease, for example, develops because the A-beta and tau proteins aggregate, which leads to neuronal dysfunction and cell death. According to Alzheimer Forschung Initiative e. V., approximately 1.2 million people suffer from this disease only in Germany. The risk to fall ill grows with increasing age.

Scientists in the Department of Cellular Biochemistry at the Max Planck Institute of Biochemistry, headed by F.-Ulrich Hartl, now established a novel experimental model aimed at elucidating cellular protein misfolding and discovered why the misfolding and aggregation are deleterious for cells. They prepared several artificial aggregating proteins without any biological function and introduced them into cells. These model proteins clumped together, coaggregating many natural proteins and, in that way, disturbing their function. By means of quantitative proteomics, the researchers discovered that the affected proteins share certain structural characteristics which predispose them for the co-aggregation: They are large in size, less hydrophobic and show a significant increase of disorder in their structure.

Protien Folding Video

“These are proteins that have not only many, but also very important functions in the cell”, explains Martin Vabulas. “For instance, they are responsible for the stability of the cytoskeleton, the organization of the chromatin in nucleus, the transcription of DNA to RNA or the synthesis of proteins. Simultaneous disturbance of several of these essential processes is most probably the reason of the cellular break-down. As a consequence, protein misfolding diseases develop.”

Molecular chaperones could possibly prevent this dire scenario. They are able to shield the aggregates, so that the aggregates cannot get in touch with other proteins anymore. The scientists hope that their new insights might help to develop novel therapeutic strategies in the battle against neurodegenerative diseases, especially at the earlier stages, before the irreversible collapse of cellular protein network sets in.

http://www.biochem.mpg.de/en/news/pressroom/index.html

• Full bibliographic informationAmyloid-like Aggregates Sequester Numerous Metastable Proteins
  with Essential Cellular Functions
  Heidi Olzscha,1,4 Sonya M. Schermann,1,4 Andreas C. Woerner,1 Stefan Pinkert,1 Michael H. Hecht,2 Gian G. Tartaglia,3,5
  Michele Vendruscolo,3 Manajit Hayer-Hartl,1,* F. Ulrich Hartl,1,* and R. Martin Vabulas1,*
  1Department of Cellular Biochemistry, Max Planck Institute of Biochemistry, Am Klopferspitz 18, D-82159 Martinsried, Germany
  2Department of Chemistry, Princeton University, Princeton, NJ 08544, USA
  3Department of Chemistry, University of Cambridge, Lensfield Road, Cambridge CB2 1EW, UK
  4These authors contributed equally to this work
  5Present address: Bioinformatics & Genomics Program, CRG Centre for Genomic Regulation, Dr. Aiguader 88, Barcelona 08003, Spain
  *Correspondence: mhartl@biochem.mpg.de (M.H-H.), uhartl@biochem.mpg.de (F.U.H.), vabulas@biochem.mpg.de (R.M.V.)
  DOI 10.1016/j.cell.2010.11.050

Technorati Tags: Alzheimer’s, Huntington’s chorea, Parkinson’s, polypeptides

The millions of people who spend hours every day on a cell phone, may have a new excuse for yakking.  A surprising new study in mice provides the first evidence that long-term exposure to electromagnetic waves associated with cell phone use may actually protect against, and even reverse, Alzheimer’s disease. The study, led by University of South Florida researchers at the Florida Alzheimer’s Disease Research Center (ADRC), was published today in the Journal of Alzheimer’s Disease.

Technorati Tags: alzheimer's disease, Cell Phones