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Monthly Archives: November 2014
Alzheimer’s disease [AD] is the most common cause of dementia in North America. Despite 30+ years of intense investigation, the field lacks consensus regarding the etiology and pathogenesis of sporadic AD, and therefore we still do not know the best strategies for treating and preventing this debilitating and costly disease. However, growing evidence supports the concept that AD is fundamentally a metabolic disease with substantial and progressive derangements in brain glucose utilization and responsiveness to insulin and insulin-like growth factor [IGF] stimulation. Moreover, AD is now recognized to be heterogeneous in nature, and not solely the end-product of aberrantly processed, misfolded, and aggregated oligomeric amyloid-beta peptides and hyperphosphorylated tau. Other factors, including impairments in energy metabolism, increased oxidative stress, inflammation, insulin and IGF resistance, and insulin/IGF deficiency in the brain should be incorporated into all equations used to develop diagnostic and therapeutic approaches to AD. Herein, the contributions of impaired insulin and IGF signaling to AD-associated neuronal loss, synaptic disconnection, tau hyperphosphorylation, amyloid-beta accumulation, and impaired energy metabolism are reviewed. In addition, we discuss current therapeutic strategies and suggest additional approaches based on the hypothesis that AD is principally a metabolic disease similar to diabetes mellitus. Ultimately, our ability to effectively detect, monitor, treat, and prevent AD will require more efficient, accurate and integrative diagnostic tools that utilize clinical, neuroimaging, biochemical, and molecular biomarker data. Finally, it is imperative that future therapeutic strategies for AD abandon the concept of uni-modal therapy in favor of multi-modal treatments that target distinct impairments at different levels within the brain insulin/IGF signaling cascades.
‘Silent epidemic’ already striking Western New York
Joseph Giel, 90, closes his eyes to recall something while he takes a mini-mental status exam at the UC Davis Alzheimer’s Disease Center in Sacramento, Calif. Past testing has shown Giel to be in good cognitive shape.Joseph Giel, 90, closes his eyes to recall something while he takes a mini-mental status exam at the UC Davis Alzheimer’s Disease Center in Sacramento, Calif. Past testing has shown Giel to be in good cognitive shape. McClatchy Newspapers
By Melinda Miller | News Staff Reporter | Google+
on May 30, 2014 – 7:30 PM
The first winds of the “silent epidemic” of dementia already are hitting Western New York and it will get worse before it gets better, local observers say.
“In the eight Western New York counties, we estimate about 55,000 people have Alzheimer’s or another form of dementia,” said Leilani Joven Pelletier, executive director of the regional chapter of the national Alzheimer’s Association. “We’re an older community here, which naturally increases our prevalence of the illness a little bit.”
The state Health Department expects the number of dementia patients to increase by about 8 percent by 2020, and by 2025, when the front line of the “gray tsunami” of baby boomers reaches 74 – the average age of onset for Alzheimer’s – the increase will be 20 percent.
But there is no need to look ahead. The demand for help and treatment is already here.
The Alzheimer’s Disease and Memory Disorders Center, a clinic and research facility operated through the University at Buffalo’s neurology department, opened in late 2011 on the Buffalo Niagara Medical Campus and already has a satellite clinic in Williamsville.
Dr. Kinga Szigeti, director of the center, said that the clinics have seen a change in their clientele in the short time they have been open, and she credits a better-informed public for the difference.
“Initially, the patients were largely people in mid to advanced stages of Alzheimer’s, but now we are getting more people with mild symptoms that might respond better to treatment,” she said. “With current medications we can change the slope of the decline. This is a very good change in our clinical practice.”
The success of early treatment in slowing the illness has helped some people overcome their avoidance of seeing a physician and receiving the frightening diagnosis.
“People realize that the decline rate can be cut in half,” Szigeti said. “With treatment, people are staying in ‘mild’ stages for many years. They can go to their grandchildren’s graduations, they can be active, they can be happy. Just by coming in early, the nursing home could be delayed by as much as two years.”
Delay, however, does not mean cure, and right now no cure exists.
“As far as science knows right now, exercise, healthy eating, lifelong learning, those types of things may reduce the incidence of Alzheimer’s somewhat, but the real risk factor is age,” said Pelletier of the Alzheimer’s Association.
Because the illness attacks the brain and memory functions, she said, it is believed that the best way to stave off its effects is by managing other diseases that affect brain function: heart disease, diabetes, high blood pressure.
International studies support those recommendations. ““New Insights Into the Dementia Epidemic,” a report in the February New England Journal of Medicine, evaluated the results of several research projects that indicate while the actual numbers of dementia cases will almost certainly increase as more people reach old-old age (over 80 years), the percentage of cases appears to be going down by as much as 4 percent.
The decrease was attributed to a generally healthier, better educated population and particularly to a measured reduction in vascular disease – meaning heart problems and stroke.
That remains only part of the puzzle, however.
At the UB center, researchers are focusing on the hereditary indicators for dementia.
“Genetics is a very useful tool to crack this disease,” Szigeti said. “Alzheimer’s is highly heritable – about 70 percent of cases.”
By defining genetic markers for the illness, she said, researchers and ultimately physicians will be able to tailor treatments to individual patients.
“It won’t be one simple solution,” Szigeti said. “It will be part of the battery of factors we consider. I imagine treatment will turn out like what we do for colon cancer: you turn 50 and get a colonoscopy. With this, you go in at 65 and get your dementia testing.”
Those tests could involve simple cognitive exercises, genetic evaluation of skin cells and even the “smell” test. Part of the UB research is examining olfactory receptors in the genome – Szigeti explained there are “smell receptors” on every chromosome – to look for correlations between variations in the receptors and the effectiveness of dementia medications.
That is just one of many problems researchers hope to solve. For all of them, though, one of the biggest difficulties continues to be funding.
UB has received money from the National Institutes of Health, the Alzheimer’s Association, the Community Foundation for Greater Buffalo along with other smaller grants, Szigeti said, and more would be better. She noted that, since the federal cutbacks, NIH funding has been cut about 74 percent, from the top 20 proposals to the top five.
“Money always helps. It accelerates the research. If I have four people working, and can add a fifth person to help analyze the data, it could go 20 percent faster,” she said.
Pelletier was even more blunt about the facts of funding.
“Alzheimer’s costs this country $214 billion per year,” she said, “and the government gives $566 million to research (about 0.25 percent).”
“The kind of movement we need is not going to come from some office in the capital. People need to start it,” she said.
For right now, families and individuals looking for help dealing with Alzheimer’s can call UB’s Alzheimer’s Disease and Memory Disorders Center at 859-3484 for information about treatment or to participate in research. For help in coping with the symptoms and day-to-day aspects of the disease, call the Western New York chapter of the Alzheimer’s Association at (800) 272-3900. Counselors there can offer advice on interacting with an Alzheimer’s sufferer, home security measures that are available to protect patients, and support groups for both patients and caregivers, among other things.
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Vitamin D deficiency predicts cognitive decline in older men and women
The Pro.V.A. Study
Elena D. Toffanello, MD,
Alessandra Coin, MD,
Egle Perissinotto, ScD,
Sabina Zambon, MD,
Silvia Sarti, MD,
Nicola Veronese, MD,
Marina De Rui, MD,
Francesco Bolzetta, MD,
Maria-Chiara Corti, MD, MSH,
Gaetano Crepaldi, MD,
Enzo Manzato, MD and
Giuseppe Sergi, MD
| + SHOW FULL DISCLOSURES
From the Department of Medical and Surgical Sciences (Department of Medicine–DIMED), Geriatrics Division (E.D.T., A.C., S.S., N.V., D.R.M., F.B., E.M., G.S.), and Departments of Cardiac, Thoracic and Vascular Sciences (E.P.) and Medical and Surgical Sciences (S.Z.), University of Padova; National Research Council (S.Z., G.C., E.M.), Aging Branch, Institute of Neuroscience, Padova; and Azienda Unità Locale Socio Sanitaria 16 (M.-C.C.), Padova, Italy.
Correspondence to Dr. Toffanello: firstname.lastname@example.org
Published online before print November 5, 2014, doi: http://dx.doi.org/10.1212/WNL.0000000000001080Neurology 10.1212/WNL.0000000000001080
Full Text (PDF)
Objective: To test the hypothesis that hypovitaminosis D is associated with a higher risk of cognitive decline over a 4.4-year follow-up in a large sample of older adults.
Methods: This research was part of the Progetto Veneto Anziani (Pro.V.A.), an Italian population-based cohort study of 1,927 elderly subjects. Serum 25-hydroxyvitamin D (25OHD) levels were measured at the baseline. Global cognitive function was measured with the Mini-Mental State Examination (MMSE); scores lower than 24 were indicative of cognitive dysfunction, and a decline of 3 or more points on the MMSE over the follow-up was considered as clinically significant. Analyses were adjusted for relevant confounders, including health and performance status.
Results: Participants with 25OHD deficiency (<50 nmol/L) or insufficiency (50–75 nmol/L) were more likely to have declining MMSE scores during the follow-up than those who were 25OHD sufficient (≥75 nmol/L). Among participants cognitively intact (baseline MMSE scores ≥24 and without diagnosis of dementia), the multivariate adjusted relative risk (95% confidence interval [CI]) of the onset of cognitive dysfunction was 1.36 (95% CI: 1.04–1.80; p = 0.02) for those with vitamin D deficiency and 1.29 (95% CI: 1.00–1.76; p = 0.05) for those with vitamin D insufficiency by comparison with individuals with normal 25OHD levels. Conclusion: The results of our study support an independent association between low 25OHD levels and cognitive decline in elderly individuals. In cognitively intact elderly subjects, 25OHD levels below 75 nmol/L are already predictive of global cognitive dysfunction at 4.4 years. Continue reading
Low Testosterone: No consistent evidence of an increased risk of heart problems with testosterone medicines
No consistent evidence of an increased risk of heart problems with testosterone medicines
The Coordination Group for Mutual Recognition and Decentralised Procedures – Human (CMDh), a regulatory body representing EU Member States, has agreed by consensus that there is no consistent evidence of an increased risk of heart problems with testosterone medicines in men who lack the hormone (a condition known as hypogonadism). However, the product information is to be updated in line with the most current available evidence on safety, and with warnings that the lack of testosterone should be confirmed by signs and symptoms and laboratory tests before treating men with these medicines.
The CMDh position follows a review by the EMA’s Pharmacovigilance Risk Assessment Committee (PRAC) which looked at the risk of serious problems affecting the heart and circulation, particularly heart attacks, in men treated with these medicines. The review was started because of some recent studies suggesting an increase in heart problems in men using testosterone, compared with men not using it. The PRAC considered these studies along with available data from other studies and analyses, and information on safety collected since marketing, and found that the evidence regarding the risk of heart problems was inconsistent: some studies suggested increased risk, while others did not, and some of the studies had problems with the design that limited the conclusions that could be drawn from them. The PRAC also noted that the lack of testosterone itself could increase the risk of heart problems.
The PRAC recommended updating the product information in line with the latest evidence and to provide warnings about those who might be at increased risk of heart problems. The product information should make it clear that testosterone should only be used when an abnormally low level of the hormone has been confirmed by signs and symptoms and appropriate laboratory tests. Testosterone levels naturally fall somewhat with age, but restoration of these levels in healthy older men is not an authorised use of the medicine in the EU. The PRAC further considered that the risks of effects on the heart and circulation, and any potential mechanisms for such effects should continue to be monitored, and information from ongoing studies should be provided as part of the next regular safety review (to which these medicines, like all medicines in the EU, are subject).
The CMDh has endorsed the PRAC recommendations by consensus and they will now be directly implemented according to an agreed timetable by the Member States where the medicines are authorised. Continue reading
We made a pooled analysis of two case-control studies on malignant brain tumours with patients diagnosed during 1997–2003 and 2007–2009. They were aged 20–80 years and 18–75 years, respectively, at the time of diagnosis. Only cases with histopathological verification of the tumour were included. Population-based controls, matched on age and gender, were used. Exposures were assessed by questionnaire. The whole reference group was used in the unconditional regression analysis adjusted for gender, age, year of diagnosis, and socio-economic index. In total, 1498 (89%) cases and 3530 (87%) controls participated. Mobile phone use increased the risk of glioma, OR = 1.3, 95% CI = 1.1–1.6 overall, increasing to OR = 3.0, 95% CI = 1.7–5.2 in the >25 year latency group. Use of cordless phones increased the risk to OR = 1.4, 95% CI = 1.1–1.7, with highest risk in the >15–20 years latency group yielding OR = 1.7, 95% CI = 1.1–2.5. The OR increased statistically significant both per 100 h of cumulative use, and per year of latency for mobile and cordless phone use. Highest ORs overall were found for ipsilateral mobile or cordless phone use, OR = 1.8, 95% CI = 1.4–2.2 and OR = 1.7, 95% CI = 1.3–2.1, respectively. The highest risk was found for glioma in the temporal lobe. First use of mobile or cordless phone before the age of 20 gave higher OR for glioma than in later age groups.
Panic Disorder/Psychiatry Home > Medicine > Psychiatry SUBDISCIPLINES JOURNALS BOOKS SERIES TEXTBOOKS REFERENCE WORKS Panic Disorder Neurobiological and Treatment Aspects Nardi, Antonio Egidio, Freire, Rafael Christophe R (Eds.) 2015, Approx. 300 p. 20 illus., 5 illus. in color. Available Formats: eBook Information Hardcover Information approx. $189.00 (net) price for USA ISBN 978-3-319-12537-4 free shipping for individuals worldwide Due: July 25, 2015 add to marked items Tweet ABOUT THIS BOOK AUTHORS & EDITORS All updated neurobiological aspects in just one book Researchers from different countries working together Psychopharmacological aspects based on research … Continue reading
Obes Rev. 2014 Nov 17. doi: 10.1111/obr.12230. [Epub ahead of print] Do ketogenic diets really suppress appetite? A systematic review and meta-analysis. Gibson AA1, Seimon RV, Lee CM, Ayre J, Franklin J, Markovic TP, Caterson ID, Sainsbury A. Author information Abstract Very-low-energy diets (VLEDs) and ketogenic low-carbohydrate diets (KLCDs) are two dietary strategies that have been associated with a suppression of appetite. However, the results of clinical trials investigating the effect of ketogenic diets on appetite are inconsistent. To evaluate quantitatively the effect of ketogenic diets on subjective appetite ratings, we conducted a … Continue reading
Special issue on panic disorder: Actual separations and losses during childhood, such parental death, parental separation or divorce (CPL), effect lifelong alterations in the physiological reactivity of the endogenous opioid system of healthy adults.
This is the final, published version of our paper, published in the special issue of Neuroscience & Biobehavioral Reviews Volume 46, Part 3, October 2014, Pages 345–351 Translational approaches to panic disorder http://www.sciencedirect.com/science/article/pii/S0149763414000827 PDF: Preter Klein 2014 final journal version Nov 20 2014 FULLTEXT: Article outline Highlights Abstract Keywords 1. Panic and comorbid conditions 2. Testing the panic-suffocation-false alarm-endogenous opioid connection References Neuroscience & Biobehavioral Reviews Volume 46, Part 3, October 2014, Pages 345–351 Translational approaches to panic disorder Review Lifelong opioidergic vulnerability through early life … Continue reading
Went to a fabulous lecture by Dr. Souhel Najjar on autoimmune encephalitis this morning. As a reminder, bad relationships (including with one’s self-image etc.) can also cause/contribute to inflammatory burden. Below is a well-informed and written piece on Anti-NMDA-receptor encephalitis (one of many), courtesy of Wikipedia. Last edited 11 days ago by an anonymous user Anti-NMDA receptor encephalitis Watch this page Anti-NMDA (N-methyl D-aspartate) receptor antibody encephalitis, also termed NMDA receptor antibody encephalitis, is an acute form of encephalitis which is potentially lethal but has high probability for … Continue reading