Alzheimer's - Dementia, Author Interviews, Sleep Disorders / 29.10.2014

Christian Benedict PhD Associate Professor of Neuroscience Uppsala University Dept. of NeuroscienceMedicalResearch.com Interview with: Christian Benedict PhD Associate Professor of Neuroscience Uppsala University Dept. of Neuroscience   Medical Research: What is the background for this study? Answer: Our study involved ~1500 men who were followed from 1970 to 2010. All participants were 50 years old at the start of study. Medical Research: What are the main findings? Answer: Men with reports of sleep disturbances had a 50%-higher risk to develop Alzheimer's disease during the 40-year follow-up period, than men without reports of sleep disturbances.
Alzheimer's - Dementia, Author Interviews, BMJ / 10.09.2014

Sophie Billioti de Gage PharmD University of Bordeaux Segalen FranceMedicalResearch.com Interview with: Sophie Billioti de Gage PharmD University of Bordeaux Segalen France   Medical Research: What are the main findings of the study? Answer: The risk of Alzheimer’s disease was found increased by 43-51% in persons (>65) having initiated a treatment with benzodiazepines in the past (>5 years before). Risk increased with the length of exposure and when long acting benzodiazepines were used.
Alzheimer's - Dementia, Author Interviews, Cannabis / 03.09.2014

Chuanhai Cao Ph.D. Neuroscientist at the Byrd Alzheimer's Institute and the USF College of Pharmacy.MedicalResearch.com Interview with: Chuanhai Cao Ph.D. Neuroscientist at the Byrd Alzheimer's Institute and the USF College of Pharmacy. Medical Research: What are the main findings of the study? Dr. Cao: The major goal of this study was to investigate the effect of Ä9-tetrahydrocannabinol (THC), a major component of marijuana, on Alzheimer’s disease (AD) pathology. THC has long been known to have anti-inflammatory effects, but we were looking to determine whether THC directly affected amyloid beta (Aâ). Aâ aggregation is considered one of the key pathological hallmarks of Alzheimer’s disease. Our study showed that extremely low doses of THC were able to decrease Aâ production, inhibit Aâ aggregation, and enhance mitochondrial function in a cellular model of AD. Decreased levels of amyloid beta, coupled with THC’s inhibitory effect on aggregation may protect against the progression of Alzheimer’s disease.
Alzheimer's - Dementia, Author Interviews, Mayo Clinic / 25.07.2014

Dr. Bryan K. Woodruff Assistant Professor of Neurology Mayo Clinic, ArizonaMedicalResearch.com Interview Invitation Dr. Bryan K. Woodruff Assistant Professor of Neurology Mayo Clinic, Arizona Medical Research: What are the main findings of the study? Dr. Woodruff: There is evidence in the medical literature supporting a negative impact of losing a spouse for health conditions such as cancer or cardiovascular disease, but this has not been evaluated in terms of the impact of widowhood on the development of dementia.  We used the National Alzheimer’s Disease Coordinating Center (NACC) database, which pools data gathered by multiple federally-funded Alzheimer’s disease research centers to try to answer this question.  Specifically, we looked at the age at which individuals ultimately developed dementia in both individuals who lost their spouse and in those who remained married over the course of the study.  Surprisingly, the data we analyzed did not support a negative impact of losing a spouse in individuals who had no cognitive difficulties when they entered the study, and we saw a paradoxical effect of widowhood in those with mild cognitive impairment (MCI).
Author Interviews, Mayo Clinic, Neurology, Stroke / 06.05.2014

Kejal Kantarci, M.D. M.S. Professor of Radiology Division of Neuroradiology Mayo Clinic, Rochester, MN 55905 MedicalResearch.com Interview with: Kejal Kantarci, M.D. M.S. Professor of Radiology Division of Neuroradiology Mayo Clinic, Rochester, MN 55905 MedicalResearch: What are the main findings of the study? Dr. Kantarci: Microinfarcts are one of the most common pathologies identified in the brains of older individuals and they impact cognition. However they are invisible lesions on MRI. We demonstrated that presence of microinfarcts in autopsied individuals are associated with the macroinfarcts identified on their MRI scans than they were alive. We also demonstrated that the presence of these invisible lesions are related to greater brain atrophy rates that are localized to watershed zones.
Alzheimer's - Dementia, Author Interviews, Cognitive Issues / 12.04.2014

Ioannis Tarnanas M.Sc Senior Researcher Gerontechnology and Rehabilitation Research Group, ARTORG Centre for Biomedical Engineering, University of Bern, 3010 Bern, SwitzerlandMedicalResearch.com Interview with: Ioannis Tarnanas M.Sc Senior Researcher Gerontechnology and Rehabilitation Research Group, ARTORG Centre for Biomedical Engineering, University of Bern, 3010 Bern, Switzerland MedicalResearch.com: What are the main findings of the study? Answer: We examined 75 healthy older people and 134 patients with mild cognitive impairment. Our aim was to collect neuropsychological, neurophysiological, neuroimaging and behavioural data by means of a virtual reality serious game, in order to model the profile of the patients who will progress to dementia within the next 2-4 years. We found that the prediction based on the performance at the virtual reality based computerized assessment instrument is comparable to that of more established and widely accepted biomarkers, such as ERP and MRI. This can be explained by the cognitive fidelity and richness of behavioural data collected with virtual reality based measures, which directly reflect neurocognitive processes affected at a very early stage.
Alzheimer's - Dementia, Author Interviews, Nature / 05.12.2013

Alessandra d’Azzo PhD Department of Genetics, St Jude Children’s Research Hospital 262 Danny Thomas Place, Memphis, Tennessee 38105MedicalResearch.com Interview with: Alessandra d’Azzo PhD Department of Genetics, St Jude Children’s Research Hospital 262 Danny Thomas Place, Memphis, Tennessee 38105 MedicalResearch.com: What are the main findings of the study? Dr. d’Azzo: We have discovered a connection between a rare childhood disorder and Alzheimer’s disease that usually affects older people. The culprit is a metabolic enzyme called NEU1 that normally controls the recycling or disposal of proteins in a specific cell compartment, the lysosome. When NEU1 is defective, children develop the severe metabolic disease, sialidosis. Our study suggests that NEU1 also plays an important role in the development of Alzheimer’s disease. Based on this discovery, we decided to increase NEU1 enzyme activity in the brain of an Alzheimer’s disease mouse model that shows features characteristic of the human disease, namely the accumulation of toxic protein aggregates or plaques. Remarkably, we could significantly diminish the number of plaques in the brain of these mice by increasing NEU1 enzyme activity.
Alzheimer's - Dementia, Author Interviews / 24.10.2013

MedicalResearch.com Interview with: Andrew S. Lim MD MMSc FRCPC DABPN Assistant Professor and Clinician Scientist Division of Neurology, Department of Medicine Sunnybrook Health Sciences Centre University of Toronto MedicalResearch.com: What are the main findings of the study? Dr. Lim: Alzheimer disease (AD) is the result of a confluence of genetic, behavioral, and environmental risk factors.  The Apolipoprotein E (APOE) e4 allele is the most common and well established genetic risk factor for Alzheimer Disease.  10-20% of the US population carries the high risk APOE e4 allele, which confers up to a 30% lifetime risk of AD. Meanwhile, previous work had suggested that poor sleep may be a risk factor for AD and that APOE genotype and poor sleep may amplify each other's negative cognitive effects. We asked the question whether good sleep consolidation (i.e. sound sleep without repeated awakenings) may reduce the effect of APOE on the risk of incident AD and the burden of AD pathology.  We studied 698 individuals without dementia participating in the Rush Memory and Aging Project - a longitudinal cohort study of aging and risk factors for AD.  We measured sleep consolidation using wrist-watch like devices called actigraphs, and followed participants for up to 6 years, examining them annually for the development of AD.  Autopsies were perfumed on 201 participants who died during the follow-up period and we quantified the burden of AD pathology. During the follow-up period, 98 participants developed AD.  As expected, carrying the APOE e4 allele was associated with a higher risk of AD, faster cognitive decline, and a higher burden of AD pathology (amyloid plaques and neurofibrillary tangles) at death. However, better sleep at baseline significantly reduced the negative impact of APOE e4 on the risk of AD, rate of cognitive decline, and burden of neurofibrillary tangle pathology.
Alzheimer's - Dementia, Author Interviews / 03.10.2013

MedicalResearch.com Interview with: Keiichi Yamamoto, MD, PhD Department of Geriatric Medicine and Neurology, Osaka City University Graduate School of Medicine Osaka, Japan. MedicalResearch.com: What are the main findings of the study? Answer: Aβ is normally bound to and transported by albumin in blood. We therefore hypothesized that decreased blood levels of Albumin-Aβ complexes may be associated with decreased Aβ removal from brain to blood, resulting in Aβ accumulation in the brain. This is the first study demonstrated that decreased serum level of albumin-Aβ complexes was strongly associated with a higher prevalence of Alzheimer’s disease (AD). This association was independent of age, sex, and ApoE4 allele. In addition, decreased serum level of albumin-Aβ complexes was correlated with decreased levels of Aβ42 in the CSF and increased levels of p-tau in the CSF, findings that have been shown to be associated with specific neuropathologic findings and AD progression.
Alzheimer's - Dementia, Author Interviews, Genetic Research, Nature / 16.08.2013

MedicalResearch.com Interview with: Steve Estus PhD Dept. of Physiology University of Kentucky Office: Room 332 Sanders-Brown Building 800 S. Limestone Street Lexington, KY 40536-0230 MedicalResearch.com: What are the main findings of the study? Answer: We report evidence for the function of a Alzheimer's genetic  risk factor.  This protective allele of the polymorphism decreases the splicing efficiency of exon 2 in CD33, a receptor protein that regulates microglial activation.  Loss of exon 2 appears to produce a dormant CD33 protein, resulting in increased microglial phagocytosis activity.  Overall, these findings confirm and extend recent papers in Neuron and Nature Neuroscience  (discussed further in our report) that described decreased CD33 activity with the protective SNP allele.
Author Interviews, Mental Health Research, Nature / 12.04.2013

MedicalResearch.com eInterview: Professor Nigel S. Scrutton ScD FRSC FSB Director Manchester Institute of Biotechnology EPSRC Established Career Fellow |Faculty of Life Sciences | Manchester Institute of Biotechnology | University of Manchester | Manchester | M1 7DN | UK | MedicalResearch.com: What are the main findings of your study? Dr. Scrutton: A major breakthrough has been made by our team of researchers seeking treatments for degenerative illnesses such as Parkinson's Disease. We have detailed how an enzyme in the brain interacts with a drug-like lead compound directed against Huntington's Disease (but also with major implications for Alzheimer’s and Parkinson’s diseases) to inhibit its activity. The work – which solved the molecular structure of a crucial brain enzyme called kynurenine 3-monooxygenase – opens the door to effective treatment for neurodegenerative diseases such as Huntington's, Alzheimer's and Parkinson's. The main findings not only describe the molecular details of the enzyme, but also how it interacts with a lead drug compound that inhibits the natural activity of the enzyme.