
One of the complications from diabetes is blindness known as diabetic macular edema (DME). DME is characterized by swelling of the central portion of the retina (or macula) at the back of the eye. It is one of the most common causes of blindness, which occurs when fluid and protein deposits collect on or under the macula–causing it to thicken and swell.
Barbara Araneo, PhD, director of Johns Hopkins’ complications program, evaluated 126 diabetic patients (average age 62 years) with Diabetic Macular Edema in a 6-month study. Patients were randomly assigned to receive one of 3 treatments.
Patients treated with ranibizumab experienced significantly greater improvements in clarity of vision and a 56% reduction in excess retinal thickness. On average the ranibizumab medicated patients showed improved vision from 20/80 to 20/63. Patients receiving the laser treatment alone, or in combination with medication, showed no visual clarity improvement.
Men and women differ on their risk of developing Alzheimer’s disease.
French researchers studied nearly 7,000 people over 65 years from the general population of 3 French cities. None of the subjects had dementia, but 4 out of 10 had mild cognitive impairment at the onset of the study. At 2 and 4 years the participants were re-evaluated.
Why diabetic patients are more likely to develop Alzheimer’s disease has not been understood. Researchers believe they may have identified the diabetes - Alzheimer’s connection.
David R. Schubert, PhD, professor Cellular Neurobiology Laboratory, Salk Institute for Biological Studies, reports that blood vessels in the brain of young diabetic mice are damaged by the interaction of elevated blood glucose levels characteristic of diabetes and low levels of beta amyloid (a peptide that clumps to form a plaque in the brain associated with Alzheimer’s).
Recent studies show that both type 1 & 2 diabetic patients have a 30-65% higher risk of developing Alzheimer’s disease compared to non-diabetic individuals. Most previous studies investigating the diabetes-Alzheimer’s connection have focused on altered insulin signaling in the brain, but have paid little attention to the effects of increased blood glucose levels on brain function and the role they play in development of Alzheimer’s.
Using genetically engineered mice researchers found that vascular damage was due to overproduction of free radicals, which damage the cells lining the brain’s blood vessels. There may be a synergistic toxicity between the amyloid protein and a high level of blood glucose that is causing problems with blood vessel formation.
While this initial trial was only marginally successful a new family of drugs has shown promise for preventing Alzheimer’s disease and perhaps the vascular damage associated with diabetes.
Among nursing home residents the 2 most common medical conditions are dementia and urinary incontinence; often they coexist. The problem is that the drugs used to treat each condition are pharmacological opposites, which can reduce the effectiveness of one or both drugs.
Kaycee M. Sink, MD, MAS, Wake Forest University School of Medicine, and colleagues, studied 3,141 Indiana nursing home residents who were taking dementia medication, which included 395 residents who were taking both dementia and urinary incontinence medication. Subjects were 65 years or older.
Subjects of the study had at least 2 consecutive prescriptions for cholinesterase inhibitors–i.e. Aricept®, Razadyne®, Exelon®, Cognex®–used to treat dementia. Of the subjects in the study approximately 33% of the people with dementia also take a drug for incontinence. Approximately, 10% of the residents also took one of the 2 most commonly prescribed urinary incontinence drugs–oxybutynin or tolterodine.
Researchers found that nursing home residents who took medications for dementia and incontinence at the same time had a 50% faster decline in function than those who were being treated only for dementia.
Also noted by researchers is that their study was conducted between 2003 and 2004, which is before newer incontinence medications were introduced that may have less of an effect on the brain.
A relatively new and effective class of oral antidiabetic agents, thiazolidinediones, have gained in popularity and widely used to treat diabetic patients with insulin resistance. Two of the more popular drugs from this class are prioglitazone and rosiglitazone, which account for 21% of oral diabetes medications prescribed in the United States and 5% of those in Europe.
Christian Meier, MD, University Hospital Basel, Basel, Switzerland studied 1,020 during a 11 year period ending in 2005. After adjusting for various risk factors researchers found that individuals taking rosiglitazone or pioglitazone had approximately double to triple the odds of hip, wrist, and other non-spine fractures, when compared to other diabetic drug treatments.
Parkinson’s disease (PD) is a progressive brain disorder that affects motor skills, which worsen as the disease advances. It is thought that in the early stages of the disease the brain begins to reduce the amount of the neurotransmitter dopamine. The reduced amount of dopamine results in trembling in the hands, arms, legs, and jaw. There is also stiffness of the limbs, slowness of movement, and impaired balance and coordination.
Roy A. E. Bakay, MD, neurosurgeon, Rush University Medical Center, used a novel approach to treat Parkinson’s disease consisting of Spheramineretinal (pigment epithelial (RPE) cells attached to tiny gelatin bead microcarriers implanted in the brain).
Six patients with moderate to advanced Parkinson’s disease were given Spheramine implants. All participants were monitored for at least 4 years and up to 6 years. Researchers report the subjects showed long-term improvement or stabilization of their symptoms for a minimum of 2 years after the Spheramine implantation. No serious Spheramine related adverse effects were reported. (Headaches were reported for 1 or 2 weeks after surgery.)
After a visit to the doctors office you want to believe that his or her diagnosis is accurate because it means you now have a path for recovery. The question is how often do doctors misdiagnose a patient’s symptoms?
The May issue of The American Journal of Medicine has a collection of articles relating to misdiagnoses and suggest that for specialties like pathology, radiology, and dermatology the misdiagnosis is less than 5%, but in many other areas misdiagnosis can be in the range of 10-15%.
Because misdiagnosis is a sensitive topic it is rarely discussed or studied. The lack of information regarding misdiagnosis can result in a physician failing to realize that it occurs far more often than they think.
Misdiagnosis is partly the result of medical practitioners failing to use systems designed to aid their diagnostic decision making. Paul Mongerson, creator of a foundation to promote computer-based diagnostic strategies writes, “In my view, diagnostic error will be reduced only if physicians have a more realistic understanding of the amount of diagnostic errors they PERSONALLY make…I believe that the accuracy of diagnosis can be best improved by informing physicians of the extent of their own (not others) errors and urging them to personally take steps to reduce their own errors.”
Dementia is an umbrella term used to describe various cognitive degenerative diseases. A common form of dementia is Alzheimer’s disease. A relatively rare hereditary form of dementia is frontotemporal dementia (FTD) with parkinsonism-17. Both of these forms of dementia share a common pathology–an over accumulation of tau proteins, which form tangled lesions in the brain’s neurons which eventually lead to the collapse of the brain cells responsible for memory.
Kun Ping Lu, MD, PhD, scientist, Division of Hematology/Oncology, Beth Israel Deaconess Medical Center (BIDMC) reports that the enzyme Pin1, which has been shown to ‘detangle’ the tau protein in Alzheimer’s, may actually have the reverse effect and accelerate dementia in the FTD form of the disease.
Researchers found that when Pin1 was present the tau proteins readily degraded. When the Pin1 enzyme was removed the tau proteins failed to break down.
When the experiment was performed on mice that were genetically engineered to model either the over-expressed Pin1 enzyme or model Alzheimer’s disease researchers were astonished at the result. Not only did the exact same Pin1 over-expression not suppress tau stability, it actually increased the tau protein’s neurodegenerative activity.
Researchers suggest their findings show that they established proof that Pin1 activity may offer a new approach for treatment of Alzheimer’s disease. Also, Alzheimer’s researchers should avoid using mice models that include P301L tau along with Alzheimer’s disease model.
Bullying is most often discussed as being an adolescence issue and left behind once out of high school. Research now indicates that effects of bullying may linger well into early adulthood.
Allison Dempsey, doctoral student, University of Florida College of Education, studied the effects of bullying on 210 college students. Primarily, Dempsey asked participants about their experiences during high school to see if there were any links with a current sense of loneliness, depression, and anxiety. She found there is a link between adolescence victimization and developing depression and anxiety in early adulthood.
Rather than physical threats alone, Dempsey included rumors, gossip, and social shunning as tactics of bullies because of their relationship with psychological symptoms.
Co-author, Eric Storch, PhD, assistant professor of psychiatry, University of Florida College of Medicine, was also interested if ‘friends’ mitigated the effects of bullying. He found that:
Dempsey graduated from Columbine High School a year before the shootings took place and now studies school prevention programs. She feels that many people see bullying and victimization as a passage of rite in high school and because of the complexity of the problem one that is difficult to stop. However, reducing the problem will help a tremendous amount.
For years tobacco company advertisements suggested that smoking would help a person to relax. Now researchers suggest that smoking will also increase a person for the risk of depression.
Almudena Sánchez-Villegas, professor, University of Navarra, based his research on a 6 year study of 8,556 university graduates (average age of 42) over a 6 year period. During the study 190 smokers, who initially did have signs of depression, were diagnosed with the disease. Also, 65 participants who had been diagnosed with depression indicated they were taking antidepressants at some point during the study period. Overall, smokers have a 41% higher risk of suffering from depression according to the study.
Sánchez-Villegas suggest that both environmental and genetic influences are factors that determine if a person will use a tobacco product, which are also possible factors that may increase the risk the individual will suffer from depression.