Alzheimer's disease is one of the most significant healthcare problems nationally and globally. Recently, the first description of the reversal of cognitive decline in patients with early Alzheimer's disease or its precursors, MCI (mild cognitive impairment) and SCI (subjective cognitive impairment), was published [1]. The therapeutic approach used was programmatic and personalized rather than monotherapeutic and invariant, and was dubbed metabolic enhancement for neurodegeneration (MEND). Patients who had had to discontinue work were able to return to work, and those struggling at work were able to improve their performance. The patients, their spouses, and their co-workers all reported clear improvements. Here we report the results from quantitative MRI and neuropsychological testing in ten patients with cognitive decline, nine ApoE4+ (five homozygous and four heterozygous) and one ApoE4-, who were treated with the MEND protocol for 5-24 months. The magnitude of the improvement is unprecedented, providing additional objective evidence that this programmatic approach to cognitive decline is highly effective. These results have far-reaching implications for the treatment of Alzheimer's disease, MCI, and SCI; for personalized programs that may enhance pharmaceutical efficacy; and for personal identification of ApoE genotype.
Showing posts with label protection. Show all posts
Showing posts with label protection. Show all posts
How to prevent Alzheimer's disease and dementia
Researchers say there are certain lifestyle measures we can take to reduce our risk of developing Alzheimer's disease and dementia, including being physically active, eating a healthy and balanced diet, maintaining good cardiovascular health, and exercising the brain.
Pathology supported genetic testing and treatment of cardiovascular disease in middle age for prevention of Alzheimer's disease.
Chronic, multi-factorial conditions caused by a complex interaction between genetic and environmental risk factors frequently share common disease mechanisms, as evidenced by an overlap between genetic risk factors for cardiovascular disease (CVD) and Alzheimer's disease (AD). Single nucleotide polymorphisms (SNPs) in several genes including ApoE, MTHFR, HFE and FTO are known to increase the risk of both conditions. The E4 allele of the ApoE polymorphism is the most extensively studied risk factor for AD and increases the risk of coronary heart disease by approximately 40%. It furthermore displays differential therapeutic responses with use of cholesterol-lowering statins and acetylcholinesterase inhibitors, which may also be due to variation in the CYP2D6 gene in some patients. Disease expression may be triggered by gene-environment interaction causing conversion of minor metabolic abnormalities into major brain disease due to cumulative risk. A growing body of evidence supports the assessment and treatment of CVD risk factors in midlife as a preventable cause of cognitive decline, morbidity and mortality in old age. In this review, the concept of pathology supported genetic testing (PSGT) for CVD is described in this context. PSGT combines DNA testing with biochemical measurements to determine gene expression and to monitor response to treatment. The aim is to diagnose treatable disease subtypes of complex disorders, facilitate prevention of cumulative risk and formulate intervention strategies guided from the genetic background. CVD provides a model to address the lifestyle link in most chronic diseases with a genetic component. Similar preventative measures would apply for optimisation of heart and brain health.
Targeting ASIC1 in primary progressive multiple sclerosis: evidence of neuroprotection with amiloride.
Neurodegeneration is the main cause for permanent disability in multiple sclerosis. The effect of current immunomodulatory treatments on neurodegeneration is insufficient. Therefore, direct neuroprotection and myeloprotection remain an important therapeutic goal. Targeting acid-sensing ion channel 1 (encoded by the ASIC1 gene), which contributes to the excessive intracellular accumulation of injurious Na(+) and Ca(2+) and is over-expressed in acute multiple sclerosis lesions, appears to be a viable strategy to limit cellular injury that is the substrate of neurodegeneration. While blockade of ASIC1 through amiloride, a potassium sparing diuretic that is currently licensed for hypertension and congestive cardiac failure, showed neuroprotective and myeloprotective effects in experimental models of multiple sclerosis, this strategy remains untested in patients with multiple sclerosis. In this translational study, we tested the neuroprotective effects of amiloride in patients with primary progressive multiple sclerosis. First, we assessed ASIC1 expression in chronic brain lesions from post-mortem of patients with progressive multiple sclerosis to identify the target process for neuroprotection. Second, we tested the neuroprotective effect of amiloride in a cohort of 14 patients with primary progressive multiple sclerosis using magnetic resonance imaging markers of neurodegeneration as outcome measures of neuroprotection. Patients with primary progressive multiple sclerosis underwent serial magnetic resonance imaging scans before (pretreatment phase) and during (treatment phase) amiloride treatment for a period of 3 years. Whole-brain volume and tissue integrity were measured with high-resolution T(1)-weighted and diffusion tensor imaging. In chronic brain lesions of patients with progressive multiple sclerosis, we demonstrate an increased expression of ASIC1 in axons and an association with injury markers within chronic inactive lesions. In patients with primary progressive multiple sclerosis, we observed a significant reduction in normalized annual rate of whole-brain volume during the treatment phase, compared with the pretreatment phase (P = 0.018, corrected). Consistent with this reduction, we showed that changes in diffusion indices of tissue damage within major clinically relevant white matter (corpus callosum and corticospinal tract) and deep grey matter (thalamus) structures were significantly reduced during the treatment phase (P = 0.02, corrected). Our results extend evidence of the contribution of ASIC1 to neurodegeneration in multiple sclerosis and suggest that amiloride may exert neuroprotective effects in patients with progressive multiple sclerosis. This pilot study is the first translational study on neuroprotection targeting ASIC1 and supports future randomized controlled trials measuring neuroprotection with amiloride in patients with multiple sclerosis.
Choline Supplement Shows Promise for Preventing Schizophrenia | Brain & Behavior Research Foundation (Formerly NARSAD)
According to a new study by a research team that includes NARSAD Grantees Robert Freedman, M.D., Randal G. Ross, M.D., Sherry Leonard, Ph.D. and Karen E. Stevens, Ph.D., choline, an essential nutrient, shows promise for lowering the physiological risk of developing schizophrenia. The team at the University of Colorado Denver administered prenatal dietary supplements of choline to pregnant mothers in the last two trimesters of pregnancy and postnatal supplements to their infants.
Pleiotropic protective effects of phytochemicals in Alzheimer's disease.
Alzheimer's disease (AD) is a severe chronic neurodegenerative disorder of the brain characterised by progressive impairment in memory and cognition. In the past years an intense research has aimed at dissecting the molecular events of AD. However, there is not an exhaustive knowledge about AD pathogenesis and a limited number of therapeutic options are available to treat this neurodegenerative disease. Consequently, considering the heterogeneity of AD, therapeutic agents acting on multiple levels of the pathology are needed. Recent findings suggest that phytochemicals compounds with neuroprotective features may be an important resources in the discovery of drug candidates against AD. In this paper we will describe some polyphenols and we will discuss their potential role as neuroprotective agents. Specifically, curcumin, catechins, and resveratrol beyond their antioxidant activity are also involved in antiamyloidogenic and anti-inflammatory mechanisms. We will focus on specific molecular targets of these selected phytochemical compounds highlighting the correlations between their neuroprotective functions and their potential therapeutic value in AD.
MS Relapses Reduced In Trials Of New Pill: MNT
Two studies of a new pill for multiple sclerosis (dimethyl fumarate ) suggest it may reduce relapses and disability progression in people with the more common, relapsing-remitting form of the neurological condition, which accounts for around 85% of cases.
Strawberries And Blueberries Halt Cognitive Decline In Elderly
Elderly individuals who eat plenty of strawberries and blueberries are less likely to experience cognitive decline, compared to those who rarely or never eat berries, researchers from Brigham and Women's Hospital and Harvard Medical School reported in Annals of Neurology. According to their findings, the authors explained that adding flavonoids-rich berries to elderly people's diet could delay their cognitive decline by up to two-and-a-half years.
Hypothermia protects the brain against damage during stroke
Thromboembolic stroke, caused by a blood clot in the brain, results in damage to the parts of the brain starved of oxygen. Breaking up the clot with tissue plasminogen activator (tPA) reduces the amount of damage, however, there is a very short time window when the value of the treatment outweighs the side effects. New research published in BioMed Central's open access journal Experimental & Translational Stroke Medicine shows that, during the first 24 hours after a stroke, mild hypothermia (34C) can reduce the side effects of tPA and potentially increase the window of opportunity for tPA treatment.
Commonly used vitamin could help produce 'good' cholesterol, researchers find
(Medical Xpress) -- Maintaining healthy cholesterol levels can keep heart disease, heart attack and stroke away. And a commonly used vitamin could help by increasing production of “good” cholesterol in the body, researchers at the University of Florida College of Medicine-Jacksonville have found. The findings were published recently in the journal Metabolism, Clinical and Experimental. nicotinic acid increased the activity of a gene that produces a protein
called apolipoprotein A-1, which is the major component of good
cholesterol in the blood.
Why red wine can be healthy: Probable mechanism underlying resveratrol activity uncovered
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HHMI News: Exercise Triggers Beneficial Cellular Recycling
Everyone knows exercise is good for you. We’re told time spent on the treadmill can reduce our risk of diabetes, cancer, and cardiovascular disorders. But exactly how exercise provides this protection is a bit of a mystery. A new study finds that exercise prompts cells to break down unwanted proteins and other cellular junk to produce more energy. The process, called autophagy, may explain how exercise fends off metabolic disorders like diabetes and protects against other diseases.
Stopping dementia in its tracks - without drugs
While there is, as yet, no medical treatment that can cure dementia, a new study has shown that it is possible to stop its progress without using drugs.
Septin proteins take bacterial prisoners : Nature News & Comment
Microbes that become trapped in septin cages are broken down in a stage of the cell's life cycle called autophagy.
Cranberries: you need the real thing
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