Path: csiph.com!goblin3!goblin.stu.neva.ru!panix!not-for-mail From: vjp2.at@at.BioStrategist.dot.dot.com Newsgroups: alt.support.alzheimers Subject: Sun v Alz Date: Fri, 10 Feb 2017 22:11:54 +0000 (UTC) Organization: PANIX Public Access Internet and UNIX, NYC Lines: 118 Message-ID: NNTP-Posting-Host: panix2.panix.com X-Trace: reader1.panix.com 1486764714 11863 166.84.1.2 (10 Feb 2017 22:11:54 GMT) X-Complaints-To: abuse@panix.com NNTP-Posting-Date: Fri, 10 Feb 2017 22:11:54 +0000 (UTC) User-Agent: tin/2.2.1-20140504 ("Tober an Righ") (UNIX) (NetBSD/7.0.2 (i386)) Xref: csiph.com alt.support.alzheimers:2313 [2 Aug 2016 sci.med.diseases.osteoporosis:14103] I attended a seminar by Stutzmann suggesting dantrolene and rapamycin as Alzheimer treatment. A speculative jstor gedanken experiment that perhaps too much sunless indoors causes modern prion neurodegenerative and other aging diseases? The pathogenesis of Alzheimers disease is it a lifelong "calciumopathy"? Stutzmann GE. Neuroscientist. 2007 Oct;13(5):546-59. Recent studies in AD models have identified marked dysregulations in calcium signaling and related downstream pathways, which occur long before the diagnostic histopathological or cognitive changes. Under normal conditions, intracellular calcium signals are coupled to effectors that maintain a healthy physiological state. Consequently, sustained up-regulation of calcium may have pathophysiological consequences. Indeed, upon reviewing the current body of literature, increased calcium levels are functionally linked to the major features and risk factors of AD: ApoE4 expression, presenilin and APP mutations, beta amyloid plaques, hyperphosphorylation of tau, apoptosis, and synaptic dysfunction. Dantrolene, A Treatment for Alzheimer's Disease? Li Liang, M.D.a,b and Huafeng Wei, M.D., Ph.Da, Alzheimer Dis Assoc Disord. 2015 Jan-Mar; 29(1): 1-5. Previous studies support that the disruption of endoplasmic reticulum (ER) Ca2+ via overactivation of Ryanodine receptors (RYRs) plays an important role in the pathogenesis of AD. Normalization of intracellular Ca2+ homeostasis could be an effective strategy for AD therapies. Recent preclinical studies consistently support the therapeutic effects of dantrolene in various types of AD animal models. Calcium channelopathies and Alzheimer's disease: insight into therapeutic success and failures. Chakroborty S, Stutzmann GE. Eur J Pharmacol. 2014 Sep 15;739:83-95 Multifaceted involvement of calcium signaling in the pathophysiology of Alzheimer's disease (AD), and summarize the various therapeutic options currently available to combat this disease. Genetic reduction of mammalian target of rapamycin ameliorates Alzheimer's disease-like cognitive and pathological deficits by restoring hippocampal gene expression signature. Caccamo A, De Pinto V, Messina A, Branca C, Oddo S. J Neurosci. 2014 Jun 4;34(23):7988-98 Elevated mammalian target of rapamycin (mTOR) signaling has been found in Alzheimer's disease (AD) patients and is linked to diabetes and aging, two known risk factors for AD. Novel mechanisms of calcium handling by the osteoclast Zaidi M1, Moonga BS, Adebanjo OA. Proc Assoc Am Physicians. 1999 Jul-Aug;111(4):319-27. The change in cytosolic Ca2+ is transduced finally into inhibition of bone resorption. It has been shown that a type 2 ryanodine receptor isoform, expressed uniquely in the plasma membrane, functions as a Ca2+ influx channel and possibly as a Ca2+ sensor. Ryanodine receptors are ordinarily Ca2+ release channels that have a microsomal membrane location in a wide variety of eukaryotic cells, including the osteoclasts. Sunlight and vitamin D for bone health and prevention of autoimmune diseases, cancers, and cardiovascular disease. Holick MF. Am J Clin Nutr. 2004 Dec;80(6 Suppl):1678S-88S. Solar ultraviolet B photons are absorbed by 7-dehydrocholesterol in the skin, leading to its transformation to previtamin D3, which is rapidly converted to vitamin D3. Vitamin D deficiency not only causes rickets among children but also precipitates and exacerbates osteoporosis among adults and causes the painful bone disease osteomalacia. Vitamin D deficiency has been associated with increased risks of deadly cancers, cardiovascular disease, multiple sclerosis, rheumatoid arthritis, and type 1 diabetes mellitus. Association of coronary artery calcium with bone mineral density in postmenopausal women. Xu R1, Ni Yang H, Li YQ, Wang QF, Guo AH, Ayiti A, Chen XC, Gong R, Banu G, Dang Jian L, Gao Y, Sheng K, Maimti Y. Coron Artery Dis. 2016 Jun 29 Atherosclerosis and osteoporosis (OP) are common diseases in elderly individuals and may share common pathogenetic mechanisms. The aim of this study was to investigate the association between bone mineral density (BMD) and coronary artery calcium (CAC) inpostmenopausal women. Suppression of glymphatic fluid transport in a mouse model of Alzheimer's disease. Peng W, Achariyar TM, Li B, Liao Y, Mestre H, Hitomi E, Regan S, Kasper T, Peng S, Ding F, Benveniste H, Nedergaard M, Deane R. Neurobiol Dis. 2016 Sep;93:215-25 Importantly, glymphatic failure preceded significant amyloid-? deposits, and thus, may be an early biomarker of AD. By extension, restoring glymphatic inflow and ISF clearance are potential therapeutic targets to slow the onset and progression of AD. Sleep facilitates clearance of metabolites from the brain: glymphatic function in aging and neurodegenerative diseases. Mendelsohn AR, Larrick JW. Rejuvenation Res. 2013 Dec;16(6):518-23. Xie and colleagues now report that in mice the clearance activity of this so-called "glymphatic system" is strongly stimulated bysleep and is associated with an increase in interstitial volume, possibly by shrinkage of astroglial cells. Moreover, anesthesia and attenuation of adrenergic signaling can activate the glymphatic system to clear potentially toxic proteins known to contribute to the pathology of Alzheimer disease (AD) such as beta-amyloid (Abeta). Clearance during sleep is as much as two-fold faster than during waking hours. Antibody against early driver of neurodegeneration cis P-tau blocks brain injury and tauopathy. Kondo A, Shahpasand K, Mannix R, Qiu J, Moncaster J, Chen CH, Yao Y, Lin YM, Driver JA, Sun Y, Wei S, Luo ML, Albayram O, Huang P,Rotenberg A, Ryo A, Goldstein LE, Pascual-Leone A, McKee AC, Meehan W, Zhou XZ, Lu KP. Nature. 2015 Jul 23;523(7561):431-6. Traumatic brain injury (TBI), characterized by acute neurological dysfunction, is one of the best known environmental risk factors for chronic traumatic encephalopathy and Alzheimer's disease, the defining pathologic features of which include tauopathy made of phosphorylated tau protein (P-tau). Treating TBI mice with cis antibody blocks cistauosis, prevents tauopathy development and spread, and restores many TBI-related structural and functional sequelae. - = - Vasos Panagiotopoulos, Columbia'81+, Reagan, Mozart, Pindus, BioStrategist http://www.panix.com/~vjp2/vasos.htm ---{Nothing herein constitutes advice. Everything fully disclaimed.}--- [Homeland Security means private firearms not lazy obstructive guards] [Urb sprawl confounds terror] [Phooey on GUI: Windows for subprime Bimbos] - = - Vasos Panagiotopoulos, Columbia'81+, Reagan, Mozart, Pindus, BioStrategist http://www.panix.com/~vjp2/vasos.htm ---{Nothing herein constitutes advice. Everything fully disclaimed.}--- [Homeland Security means private firearms not lazy obstructive guards] [Urb sprawl confounds terror] [Phooey on GUI: Windows for subprime Bimbos]