Only a few days left to register for the CJDSGN meeting this coming Saturday at the Jasper Hotel in Melbourne. Thank you to those who have already registered. We look forward to seeing you soon. ... See MoreSee Less
You are invited to attend a CJD Support Group Network (CJDSGN) family meeting.
Date: Saturday 19th August 2017
Time: 2pm to 5.30pm - afternoon tea will be provided
Venue: Jasper Hotel,
Address: 489 Elizabeth Street, Melbourne Vic 3000
Telephone Number: (03) 83272727
RSVP: Thursday 17th August 2017
Final numbers will be required for catering purposes by this date.
Email: firstname.lastname@example.org or call the toll free number 1800 052466
Hosted by: Suzanne Solvyns and David Ralston - representing the Committee of the CJD Support Group Network.
Special Guest: Dr Christiane Stehmann, Australian National CJD Registry.
This meeting is an informal meeting where you will have the opportunity to ask any questions, share your stories with other family members who understand the difficult journey called CJD and link in with other family members for mutual support.
For those of you who have attended meetings and conferences in the past we hope that you will also come along to help us to support the new families who unfortunately continue to have their lives touched by this monster of a disease.
This is also a good way to meet others in advance if you plan to attend the Annual National CJD Conference on 18th November 2017.
The 1800 052466 will be diverted to my mobile in case you need to make contact on the day of the meeting.
Recent publications on type 2 Diabetes (T2D) research does not imply that having T2D may lead to a person developing prion disease. It is suggesting that T2D may also be a misfolding disease, like many others, and may be transmissible in a lab setting. Deana Simpson and I, as co-chairs of the CJD International Support Alliance asked Claudio Soto to provide a lay summary on his research work in this area. His response to our request came in one day as he, like all our prion researchers, is keen to keep you the families updated with research progress.
Lay Summary - Claudio Soto Type 2 diabetes (T2D) is a highly prevalent metabolic disease characterized by chronic insulin resistance, dysfunction and death of pancreatic β-cells, leading to impaired insulin release and hyperglycemia. The cause of T2D is not completely understood, but it is suspected to be related to a combination of lifestyle and genetic factors. More than 30 million people in the United States, or 9.4 percent of the population, suffers of T2D. Although the mechanism responsible for β-cell dysfunction and death is not completely understood, compelling evidence suggest that the accumulation of misfolded aggregates of the islet amyloid polypeptide (IAPP) in the pancreas may play an important role in pancreatic damage. Misfolding and aggregation of diverse proteins and their accumulation in different organs is the hallmark of various human illnesses termed Protein Misfolding diseases, including prion diseases, as well as more than 25 other diseases, such as for example Alzheimer's, Parkinson's and systemic amyloidosis. Among these illnesses, prion diseases are unique in that the illness can be transmitted through infectious proteins, termed prions, that spread the disease by transforming the normal prion protein into the abnormal, toxic form. The mechanism of prion infectivity rely on the ability of the abnormal prion protein to replicate acting as a seed to induce the alterations of the normal prion protein. Prion replication has a striking resemblance to the process of protein aggregation in all the other protein misfolding diseases. For this reason, over 10 years ago, we proposed that these other diseases have an inherent capacity to be transmissible, like prions. Recent studies from our lab and others have shown that the pathology of various of these diseases (e.g. Alzheimer's, Parkinson's disease) can be induced in animals under experimental conditions by administration of tissue extracts containing protein aggregates. In the current article we explored whether the protein aggregates implicated in T2D might be transmissible like prions. To study this, experiments were done in pancreatic islets isolated from humans and grown in the lab, as well as in mice that were engineered to produce the human IAPP protein. Exposure of human pancreatic islets to IAPP aggregates coming from diabetic mice showed that the healthy islets began to accumulate protein aggregates. Injection of IAPP aggregates (either synthetically created in the lab or taken from the pancreas of diabetic individuals), into mice induced the accumulation of protein aggregates in the pancreas and resulted in animals with all characteristics of diabetes, including high levels of blood glucose, problems with glucose tolerance and destruction of pancreatic cells. These studies demonstrate that, like prion diseases, T2D might be transmissible under experimental conditions in the lab. However, these results should not be extrapolated to real life without additional studies, because the experimental nature of the models does not permit to conclude that these effects will happen in humans. Nevertheless, our studies point to that IAPP aggregates play an important role in diabetes and open new strategies for preventing and treating T2D. It is important to highlight that we are not saying that T2D can be acquired from patients affected by prion diseases or prion diseases taken from people affected by diabetes. There are two different diseases that appear to share some similarities, which let us to think that T2D have the potential to be transmissible like prions, but again much more studies need to be done to evaluate this possibility. www.invisiverse.com/news/defective-infectious-proteins-linked-type-2-diabetes-0179122/... See MoreSee Less
The CJDSGN will be hosting a CJD family meeting at the Kirribilli Club, Milson's Point at 2pm on Saturday 23rd September 2017. Members of the CJDSGN committee will be there to answer your questions so we hope that you will join us to share your story with others who understand the difficult journey called CJD. For those of you who have attended meetings and conferences in the past we hope you will also come along to help us to support the new families who unfortunately continue to have their lives touched by this monster of a disease. I will be sending out an invitation by email to everyone on our NSW electronic list and would appreciate if you can rsvp for catering purposes. You are very welcome to rsvp by posting on this page, email email@example.com, call 1800 052466 or PM me if you would like to attend. This is also a good way to meet others in advance if you plan to attend the annual national CJD conference on 18th November 2017 or want to find out more about an annual fun run in November. ... See MoreSee Less
Great news we now have confirmation of our international speakers for our 2017 CJD Annual National CJD conference to be hosted by the CJDSGN on 18th November in Melbourne. Professor John Collinge from the Prion Unit in London will provide information on the antibody therapy (PRN 100) that they are preparing to offer to a small number of sporadic UK patients initially. Professor Robert Will from Edinburgh UK will also join and as those of you who have seen Bob speak know, he is a wonderful source of information. His topic with be risk factors with prion disease. Associate Professor Brian Appleby, a regular and very valued speaker will provide information on prion disease including updates and improvements with diagnostic tests. Associate Professor Gianluigi Zanusso is well known for the work he has done with nasal brushing using RT-QuIC and he will update us on the possiblily of using this test on asymptomatic mutation carriers for genetic CJD. Please add 18th November 2017 to your diary. Registration will be open very shortly once we have confirmation of all speakers. ... See MoreSee Less