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Tag Archives: long-term effects
Neurology. 2005 May 24;64(10):1704-11. Risk factors for progression of brain atrophy in aging: six-year follow-up of normal subjects. Enzinger C1, Fazekas F, Matthews PM, Ropele S, Schmidt H, Smith S, Schmidt R. Author information Abstract OBJECTIVES: To determine the rate of brain atrophy in neurologically asymptomatic elderly and to investigate the impact of baseline variables including conventional cerebrovascular risk factors, APOE epsilon4, and white matter hyperintensity (WMH) on its progression. METHODS: We assessed the brain parenchymal fraction at baseline and subsequent annual brain volume changes over 6 years for 201 participants (F/M … Continue reading
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.
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.
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
Association of Childhood Adversities and Early-Onset Mental Disorders With Adult-Onset Chronic Physical Conditions
Important paper on childhood adversities an adult-age chronic medical conditions, published just before our study on endogenous opioid dysregulation after early childhood adversity in psychiatrically and physically “healthy” adults. Archives of General Psychiatry August 2011, Vol 68, No. 8 > < Previous ArticleNext Article > Original Article | Aug 2011 Association of Childhood Adversities and Early-Onset Mental Disorders With Adult-Onset Chronic Physical Conditions Kate M. Scott, PhD; Michael Von Korff, ScD; Matthias C. Angermeyer, MD, PhD; Corina Benjet, PhD; Ronny Bruffaerts, PhD; Giovanni de Girolamo, MD; Josep Maria Haro, MD, MPH, … Continue reading
Maurice Preter MD and Donald F. Klein, MD, DSc: Lifelong opioidergic vulnerability through early life separation: A recent extension of the false suffocation alarm theory of panic disorder.
“[…W]e objectively, experimentally showed a physiological link between endogenous opioid system deficiency and panic-like suffocation sensitivity in healthy adults. This is consonant with the expanded Suffocation-False Alarm Theory of panic suggesting an episodic functional endogenous opioid deficit (Preter and Klein, 1998). The specificity of the naloxone + lactate model of clinical panic should be tested using specific anti-panic components, possibly including opioidergic mixed agonist-antagonists such as buprenorphine. If specific, the naloxone + lactate effect in normal humans affords a screening method for testing putative anti-panic drugs which is currently not available. This could obviate the experimental treatment of panic disorder patients in drug development.
Our data also show for the first time that 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 result encourages epigenetic inquiry into the effects of CPL on endogenous opioid systems, and their role in resilience under extreme stress. In addition, a redefinition of what constitutes a (truly) healthy control in clinical research protocols may be called for.” Continue reading