The U.S. Food and Drug Administration on October 25 approved a second amyloid imaging agent. Flutemetamol is an F18-labeled ligand developed by GE Healthcare. It joins florbetapir, developed by Avid Pharmaceuticals/Eli Lilly and Company.
Flutemetamol differs slightly from its cousin because it is approved to report the intensity of binding to amyloid plaques in false color. This could make scans easier to read, some experts agreed. The compound will be commercially available in early 2014.
In regulatory terms, both are approved to indicate whether amyloid is present, and thereby support or refute an AD diagnosis. Neither is intended to diagnose AD on its own or replace other routine clinical tests for cognitive decline. Neither compound is approved to quantify amyloid plaques in the brain. That is something both companies are exploring.
Both agents will be made available to both neurologists and researchers. GE Healthcare has submitted an application for approval to the European Medicines Agency (EMA), and will apply in various other countries in the coming months and years. Florbetapir has already gotten EMA approval, and Lilly/Avid is seeking approval in other areas of the world.
Source: AlzForum website – 21 Nov 2013
The JPND Newsletter brings together a number of relevant JPND news stories for JPND international stakeholder communities.
Contents include highlights of JPND activities, information on JPND-supported projects as well as interviews with JPND Scientific Advisory Board members.
The second edition (November 2013) is availablehere or at the link below.
Researchers studying the natural history of Alzheimers disease are grappling with a puzzling group of volunteersamyloid-free and cognitively normal older adults who show other biomarker evidence of neurodegeneration.
Researchers studying the natural history of Alzheimers disease are grappling with a puzzling group of volunteersamyloid-free and cognitively normal older adults who show other biomarker evidence of neurodegeneration.
Source: AlzForum website – 08 Nov 2013 </time><//time>
JPND is piloting an online partnering tool as an optional support for researchers interested in responding to the 2013 JPND Annual Calls for proposals.
Two JPND Calls for proposals are due to launch in early December, with the indicative call titlesalready released in a pre-call announcement.
A "JPND Partnering Tool" is being made available from November 7th to assist potential applicants to either call in their partnering activities.
The tool allows researchers to present their research group and expertise in a closed forum, tailored for JPND, thus making it easier for research partners to locate each other and collaborate on a proposal idea.
Researchers can also register a proposal idea and get comments from expert scientists and researchers within the tool. Consortia can then be built around the idea, potentially leading to drafting a proposal on the tool.
It is believed that this tool will especially benefit early-career researchers and research groups not normally included in established consortia. Established researchers can potentially use the tool to find specific expertise which may be missing from their pre-existing consortia.
Call texts, country-specific information, FAQ etc. for both 2013 Calls will be made availableon this page on the Call launch date (early December 2013).
For more information on the tool, clickhere or on the links below.
The largest international study ever conducted on Alzheimer’s disease, the I-GAP (International Genomics Alzheimers Project) consortium has identified eleven new regions of the genome involved in the onset of the disease.
This research gives an overview of the molecular mechanisms underlying the disease, opening up to a better understanding of the pathophysiology of this disease.
These results, detailed inNature Genetics, could not have been obtained without this unique worldwide collaborative effort.
In addition to the well-established association at the APOE locus, they identified 19 genomic regions significantly associated with late-onset Alzheimers disease, 11 of which are new susceptibility loci. Their findings reinforce pathways previously implicated in Alzheimers disease pathology, including immune response, inflammation, cell migration and lipid transport pathways. They also suggest new candidate genes and pathways that may be involved in disease risk.
These 11 new confirmed genes can open new avenues in the understanding of the occurrence of Alzheimer’s disease. Thus one of the most significant associations were found in the region HLA-DRB5/DRB1 major histocompatibility complex. This finding is interesting in several ways. First, it confirms the involvement of the immune system in disease. In addition, this same region is also found associated with two other neurodegenerative diseases, multiple sclerosis and Parkinson’s disease.
About I-GAP:http://www.alz.org/news_and_events_21649.asp
University of California Irvine’s trailblazing 90+ Study, aimed at learning more about the “oldest old, will continue for at least another five years, thanks to a $9.5 million renewal grant from the US National Institute on Aging.
The 90+ Study is among the largest studies of the oldest old in the world, with clinical, pathological and genetic research being conducted on more than 1,600 participants. Results obtained thus far have provided researchers across the globe with valuable information about aging."
The UC Irvine study is among the few to look at dementia in people over age 90. With the renewed round of funding over the next five years, 90+ researchers plan to employ PET and MRI scans to address these questions: Why do many of the oldest old have Alzheimer’s or vascular pathology in their brains but not show signs of dementia? Are they in the preclinical stages of disease? Will their cognitive abilities eventually decline?
The researchers also intend to monitor blood pressure and oxygen saturation over 24-hour spans to see if dips in blood pressure, particularly during the night, or periods of fluctuation are associated with cerebral microinfarctions or other diseases of the brain that can cause dementia.
Two 2-step calls are due to launch in early December 2013, with a likely first stage (pre-proposal submission) deadline of February 2014.
The EU Joint Programme Neurodegenerative Disease Research (JPND) is implementing the priorities identified in itsResearch Strategy through a range of large-scale programmatic initiatives.
During the first phase of implementation (2012-2014), JPND anticipates the launch of JPND Joint Transnational Calls each year to address high priority areas in neurodegenerative disease research*.
JPND expects to launch two Joint Transnational Calls later this year aimed at supporting transnational collaborations in the field of neurodegenerative disease research. The 2-step calls are anticipated to launch in early December 2013, with a likely first stage (pre-proposal submission) deadline of February 2014.
Further detail will be provided here on the call launch date. However, the indicative titles of each call are provided below:
A call for European research projects for Cross-Disease Analysis of Pathways related to Neurodegenerative Diseases
The aim of the call is to establish a limited number of ambitious, innovative, multi-national and multi-disciplinary collaborative research projects that;
combine experimental approaches from fundamental, pre-clinical and/or clinical with computational approaches
perform network analyses in different neurodegenerative and other chronic diseases to elucidate the underlying mechanisms common and differing in the investigated diseases
will add value to existing research by analysing diseases across traditional clinical boundaries, thereby gaining deeper understanding of the patho-physiological mechanisms of the diseases.
A call for European research projects for Pilot Studies on Preventive Strategies related to Neurodegenerative Diseases
The aim of the call is to establish pilot initiatives to develop preventive strategies. Proposals should entail multidisciplinary studies which may focus on new paradigms for multimodal preventive interventions including culture specific aspects, on harmonisation initiatives, or on proof-of-concept, and feasibility studies. Proposals may include research-based evaluation of interventions and validation of outcome measures.
Please Note:
For both calls, JPND will pilot the use of a new online partnering tool. The tool will enable call applicants to showcase their research groups expertise, search for appropriate partners, pitch call-related ideas and draft their pre- and full-proposals online. The tool will be made available through the JPND website, and will be announced in a JPND News alert in November 2013.Sign up here for JPND website alerts.
All information regarding future JPND Call topics is indicative and subject to change.
* The JPND diseases are: Alzheimers disease (AD) and other dementias, Parkinsons disease (PD) and PD-related disorders, Prion disease, Motor neurone diseases (MND), Huntingtons Disease (HD), Spinocerebellar ataxia (SCA), Spinal muscular atrophy (SMA)
A chemical substance has been identified which shows signs of being able to halt a range of neurodegenerative diseases in mice.
Researchers at the University of Leicesters Medical Research Council Toxicology Unit, investigating prion disease in mice, have found a common feature across all types of brain cell death. Looking at the natural defence mechanisms of brain cells, they found that brain cells respond by shutting down protein production when attacked by a virus (in order to halt the viruss spread).
A range of neurodegenerative diseases involve the formation of faulty or "misfolded" proteins, and these activate similar defence mechanisms. In Parkinsons Disease it is alpha-synuclein which is the errant protein, in Alzheimers Disease it is amyloid and tau, and in the case of Huntingdons Disease it is another different protein.
The researchers believe the specific errant protein is irrelevant, because it is how cells deal with misfolded protein which is important. The presence of misfolded proteins causes brain cells to shut down protein production for a long period, eventually resulting in cell death.
The researchers believe they may be able to disrupt this process by the administration of a particular compound, thereby halting neurodegeneration; at least in mice with prion disease so far.
Research teams from Sheffield, UK and Milan, Italy looked at the factors which might explain the differences observed in speed and severity in the progression of motor neuron disease (MND).
Researchers used a scientific technique known as gene expression profiling to identify factors within motor neurones that control vulnerability or resistance to MND in order to shed light on the factors important for the speed of motor neurone injury in human patients. The research, published in the scientific journal Brain, investigated two mouse models of MND caused by an alteration in the SOD1 gene, a known cause of MND in humans. One of the strains had a rapidly progressing disease course and the other a much slower change in the symptoms of MND.
The study, funded by the Motor Neurone Disease Association, revealed new evidence at the point of onset of the disease, before muscle weakness was observed, showing key differences in major molecular pathways and the way the protective systems of the body responded, between the profiles of the rapid progressing and slow progressing models. In the case of the model with rapidly progressing MND the motor neurones showed reduced functioning of the cellular systems for energy production, disposal of waste proteins and neuroprotection. Motor neurones from the model with more slowly progressing MND showed an increase in protective inflammation and immune responses and increased function of the mechanisms that protect motor neurones from damage.
Neurobiologists from the Friedrich Miescher Institute for Biomedical Research proved that excitability protects motor neurons from degeneration in amyotropic lateral sclerosis, a rare neurodegenerative disease.
By modulating excitability researchers could influence the rate of motor dysfunction and muscle denervation, and slow the progression rate of the disease.
This is important because it points to a possible way to delay the progression of this so far incurable disease.
Their results are published online in Neuron.
