With the increased life expectancies, the number of the elderly over the age of 90 is rising worldwide. A paper published in the journal, Neurology, focused on a specific study of dementia rates in the very old. Performed in California with over 900 participants, it has shown that there are differences based on gender in risks of dementia or Alzheimer’s disease (AD) for men and women over the age of 90. For women, the chances of developing dementia double by five year increments after 90 years of age, which confirmed the fact that women over 90 are at a greater risk of dementia than men in the same age group. In dementia populations over 90 years of age, only 28 percent of men have dementia, whereas 45 percent of women suffer from the disease. However, the study has revealed that women who had consistently used their brains during their life and had received a higher education had less of a chance of developing dementia compared to those who did not have that benefit. The knowledge that women are at a greater risk than men in developing heart disease or stroke with age, both of which act as independent risk factors for dementia and intensify the symptoms of AD, may be beneficial in understanding why women over 90 are at more risk. In addition, research has shown that Alzheimer’s is also negatively affected by vascular factors, as the work Roskamp Institute scientists’ showed that vasculature damage increases in presence of amyloid. Vascular risk factors are found more frequently in women as they age, and patients in the earlier stages of AD receive a greater neurological impact than normal individuals from vascular damage. Roskamp Institute scientists are using these pieces of information along with other knowledge in order to develop new treatments for dementia.
For more details on this study, as well as additional information on Alzheimer’s disease, please visit
July 27, 2012
The Roskamp Institute researchers are in search of new treatments for traumatic brain injury (TBI) to help out the veterans of the country. An article in the New England Journal of Medicine has called attention to the number of medical aftereffects of TBI in the American soldiers returning from Iraq. This was revealed through a survey of more than 2,500 soldiers returning from Iraq. Five percent of them stated that they suffered injuries with loss of consciousness, while ten percent said they had injuries that resulted in changed mental status, and another seventeen percent reported other injuries during their deployment. Of the five percent who reported loss of consciousness and of the ten percent who reported altered mental status, 45 percent and 27 percent met the criteria for Post Traumatic Stress Disorder (PTSD), respectively.
The conclusion of the article revolved around the close link between mild TBI, experienced by the veterans from Iraq, with PTSD and physical health problems three to four months after the soldiers come home. In addition, both PTSD and depression serve as mediums for the relationship between mild TBI and physical health issues.
TBI initiates degenerative pathways; researchers at Roskamp are using this knowledge to discover which genes and proteins are connected with these pathways to seek for new treatments for TBI.
For the original article, please visit http://www.roskampinstitute.us/articles/archives/27.
For more information on TBI, please visit
July 30, 2012
Pro-inflammatory cytokine production can be beneficial to the human body, as it is part of the body’s biological response. However, overproduction of these proteins promotes the development of many deteriorating neurological diseases, such as Alzheimer’s disease (AD) and the neurological damages that are aftereffects of traumatic brain injury (TBI) and stroke. High levels of pro-inflammatory cytokines inhibit proper synaptic communication and function, which eventually leads to damages in the cortex and hippocampus of the brain.
In a study from Northwestern’s Feinberg School of Medicine and University of Kentucky, a new set of drugs have been developed that targets this issue by preventing the overproduction. These drugs target neuroinflammation, a type of brain inflammation that is believed to be a major factor in the injurious nature of diseases ranging from Alzheimer’s to Parkinson’s, as well as brain injuries. The drugs, currently represented by MW151 and MW189, have been tested in previous animal studies. MWI151 was given to a six-month old (the time at which the level of pro-inflammatory cytokines being to increase) mice that are genetically engineered to develop AD for three times a week; then, their brains were examined at eleven months of age, the time at which the conditions of AD are visible. The development of the full-blown AD was avoided as the level of cytokines had returned to normal levels and their synapses were working properly. Mice that were not given the drug still had high levels of pro-inflammatory cytokines and had synaptic malfunction. In another cases, it has also helped decrease the nerve damage caused by TBI by preventing overproduction of pro-inflammatory cytokines and blocking the activation of glia cells. Success was also met when the drug was tested in mice to prevent the development of multiple sclerosis.
Phase one of the first human clinical trial has been completed, but these current studies have shown that the therapy time window is limited, so for future clinical trials, further studies involving models of other diseases and time windows will be conducted. With this new development, the future of early therapy to prevent the development of neurological diseases and the long-term complications of TBI and strokes seems promising.
Keywords: inflammation; pro-inflammatory cytokines; drug; Alzheimer’s disease; traumatic brain injury
Sources: http://www.northwestern.edu/newscenter/stories/2012/07/brain-inflamation-drug.html http://www.jneurosci.org/content/32/30.abstract.pdf
(Early Stage Drug Treatment That Normalizes Proinflammatory Cytokine Production Attenuates Synaptic Dysfunction in a Mouse Model That Exhibits Age-Dependent Progression of Alzheimer’s Disease-Related Pathology)
July 25, 2012
With Alzheimer’s disease (AD) being the most common type of dementia among the 35 million patients suffering from dementia cases worldwide, the battle to find a drug to at least slow down this disease is becoming more urgent each day. While current medicines do ease the symptoms of AD, none of them delay, stop, or reverse the cognitive and behavioral decline of AD. In recent news, a drug called bapineuzumab, that hoped to improve the cognitive and life functions of the patients participating in the trial, has failed its first of four clinical trials. The 1,100 patients in this late-stage study have mild to moderate cases of Alzheimer’s, and each has a variation of the gene, ApoE4, which increases the chances of developing AD. About half of AD patients have this gene. Bapineuzumab is an antibody based drug that targets beta-amyloid, a protein which scientists believe to be the cause of AD. The failure of this trial may be due to the high risk patients, as well as the fact that the drug is being tested too late into the disease. Jointly created by Pfizer and Johnson & Johnson, it has been announced that Johnson & Johnson will carry out the remaining three clinical trials, with one involving ApoE4 and the other two with patients without the gene. The results of these remaining trials will be presented at a neurology conference in Sweden this September. For more details and news about this study as well as Alzheimer’s disease, please visit: http://www.washingtonpost.com/business/pfizer-alzheimers-disease-drug-fails-in-1-study-2nd-study-in-different-patients-continues/2012/07/23/gJQAB7K64W_story_1.html
Keywords: Alzheimer’s disease; bapineuzumab; ApoE4
Sources: http://www.washingtonpost.com/business/pfizer-alzheimers-disease-drug-fails-in-1-study-2nd-study-in-different-patients-continues/2012/07/23/gJQAB7K64W_story_1.html http://www.nytimes.com/2012/07/24/business/alzheimers-drug-fails-its-first-clinical-trial.htmlYou can follow updates on clinical trials at the Roskamp Institute Website: http://www.rfd
July 24, 2012
Research has shown that nearly two-thirds of dementia cases of patients over 60 in the Western Hemisphere are cases caused by Alzheimer’s disease. This correlation with age continues as the frequency of Alzheimer’s nearly doubles by five year increments after the age of 65.To gain a better understanding of this prevalence, scientists are looking into the amyloid-b precursor protein (APP) gene which has shown to have a significant effect in those with Alzheimer’s disease. Through their research, derived from 1,795 Icelandic citizens, scientists have discovered a mutation in the APP gene that safeguards individuals from cognitive deterioration and Alzheimer’s disease. Because mutations on this site (A673T allele) also prevents cognitive decline in patients without Alzheimer’s, this suggests that the two conditions may be controlled by or related through the same mechanisms.
Patients enrolled in this study were registered through the Memory Clinic at Landspitali University Hospital and the cognitive condition was assessed through the Minimum Data Set (MDS) for nursing homes. Genotypic data was then collects for the APP site A673T for all 1,763 patients. This data reveals that this site on APP is vital to the production of amyloid plaque, making it able to protect patients from the cognitive decline seen in Alzheimer’s and non-Alzheimer’s patients. These results make this mutation the first genetic variant discovered that can create a strong shield from Alzheimer’s disease. It also confirms the hypothesis that the pathogenesis of regular cognitive deterioration and Alzheimer’s disease may be partially related, suggesting that Alzheimer’s disease may be the driving force of the correlation between age and decline in cognitive function.
By Alec Waid, Intern Roskamp Institute