Explore the vast range of titles available.

Could that glass of milk affect your memory? Is that aluminum can increasing your risk for Alzheimer's disease? Can a banana be a brain booster? Everyone knows that good nutrition supports your overall health, but did you know that certain foods can protect your brain and optimize its function? In this book the author has gathered research and studies to deliver a program that can boost brain health, reducing the risk of Alzheimer's disease, stroke, and other less serious malfunctions, including low energy, poor sleep patterns, irritability, and lack of focus. The plan includes information on: The best foods to increase cognitive function and boost folate, vitamin B6, and vitamin B12 ; The dangers dairy products and meats may have on memory ; The role alcohol plays in Alzheimer's risk ; The latest research on certain toxic metals, like aluminums found in cookware, soda cans, and common antacids ; Plus, 50-75 recipes and timesaving kitchen tips.

No large trials have been done to investigate the efficacy of an intervention combining a specific compound and several lifestyle interventions compared with placebo for the prevention of cognitive decline. We tested the effect of omega 3 polyunsaturated fatty acid supplementation and a multidomain intervention (physical activity, cognitive training, and nutritional advice), alone or in combination, compared with placebo, on cognitive decline. The Multidomain Alzheimer Preventive Trial was a 3-year, multicentre, randomised, placebo-controlled superiority trial with four parallel groups at 13 memory centres in France and Monaco. Participants were non-demented, aged 70 years or older, and community-dwelling, and had either relayed a spontaneous memory complaint to their physician, limitations in one instrumental activity of daily living, or slow gait speed. They were randomly assigned (1:1:1:1) to either the multidomain intervention (43 group sessions integrating cognitive training, physical activity, and nutrition, and three preventive consultations) plus omega 3 polyunsaturated fatty acids (ie, two capsules a day providing a total daily dose of 800 mg docosahexaenoic acid and 225 mg eicosapentaenoic acid), the multidomain intervention plus placebo, omega 3 polyunsaturated fatty acids alone, or placebo alone. A computer-generated randomisation procedure was used to stratify patients by centre. All participants and study staff were blinded to polyunsaturated fatty acid or placebo assignment, but were unblinded to the multidomain intervention component. Assessment of cognitive outcomes was done by independent neuropsychologists blinded to group assignment. The primary outcome was change from baseline to 36 months on a composite Z score combining four cognitive tests (free and total recall of the Free and Cued Selective Reminding test, ten Mini-Mental State Examination orientation items, Digit Symbol Substitution Test, and Category Naming Test) in the modified intention-to-treat population. The trial was registered with ClinicalTrials.gov (NCT00672685). 1680 participants were enrolled and randomly allocated between May 30, 2008, and Feb 24, 2011. In the modified intention-to-treat population (n=1525), there were no significant differences in 3-year cognitive decline between any of the three intervention groups and the placebo group. Between-group differences compared with placebo were 0·093 (95% CI 0·001 to 0·184; adjusted p=0·142) for the combined intervention group, 0·079 (−0·012 to 0·170; 0·179) for the multidomain intervention plus placebo group, and 0·011 (−0·081 to 0·103; 0·812) for the omega 3 polyunsaturated fatty acids group. 146 (36%) participants in the multidomain plus polyunsaturated fatty acids group, 142 (34%) in the multidomain plus placebo group, 134 (33%) in the polyunsaturated fatty acids group, and 133 (32%) in the placebo group had at least one serious emerging adverse event. Four treatment-related deaths were recorded (two in the multidomain plus placebo group and two in the placebo group). The interventions did not raise any safety concerns and there were no differences between groups in serious or other adverse events. The multidomain intervention and polyunsaturated fatty acids, either alone or in combination, had no significant effects on cognitive decline over 3 years in elderly people with memory complaints. An effective multidomain intervention strategy to prevent or delay cognitive impairment and the target population remain to be determined, particularly in real-world settings. French Ministry of Health, Pierre Fabre Research Institute, Gerontopole, Exhonit Therapeutics, Avid Radiopharmaceuticals.

One of the foremost Alzheimer's dementia-care clinicians presents an individualized, step-by-step, whole-body, evidence-based approach to reversing and preventing cognitive decline, aiming to help people with dementia return to themselves and help those who are living in fear of developing dementia take good care of their current and future brain health.

Depressive symptoms may increase the risk of progressing from mild cognitive impairment (MCI) to dementia. Consumption of n-3 PUFA may alleviate both cognitive decline and depression. The aim of the present study was to investigate the benefits of supplementing a diet with n-3 PUFA, DHA and EPA, for depressive symptoms, quality of life (QOL) and cognition in elderly people with MCI. We conducted a 6-month double-blind, randomised controlled trial. A total of fifty people aged >65 years with MCI were allocated to receive a supplement rich in EPA (1·67 g EPA+0·16 g DHA/d; n 17), DHA (1·55 g DHA+0·40 g EPA/d; n 18) or the n-6 PUFA linoleic acid (LA; 2·2 g/d; n 15). Treatment allocation was by minimisation based on age, sex and depressive symptoms (Geriatric Depression Scale, GDS). Physiological and cognitive assessments, questionnaires and fatty acid composition of erythrocytes were obtained at baseline and 6 months (completers: n 40; EPA n 13, DHA n 16, LA n 11). Compared with the LA group, GDS scores improved in the EPA (P = 0·04) and DHA (P = 0·01) groups and verbal fluency (Initial Letter Fluency) in the DHA group (P = 0·04). Improved GDS scores were correlated with increased DHA plus EPA (r 0·39, P = 0·02). Improved self-reported physical health was associated with increased DHA. There were no treatment effects on other cognitive or QOL parameters. Increased intakes of DHA and EPA benefited mental health in older people with MCI. Increasing n-3 PUFA intakes may reduce depressive symptoms and the risk of progressing to dementia. This needs to be investigated in larger, depressed samples with MCI.

Mild traumatic brain injury (mTBI) secondary to blast exposure is the most common battlefield injury in Southwest Asia. There has been little prospective work in the combat setting to test the efficacy of new countermeasures. The goal of this study was to compare the efficacy of N-acetyl cysteine (NAC) versus placebo on the symptoms associated with blast exposure mTBI in a combat setting. This study was a randomized double blind, placebo-controlled study that was conducted on active duty service members at a forward deployed field hospital in Iraq. All symptomatic U.S. service members who were exposed to significant ordnance blast and who met the criteria for mTBI were offered participation in the study and 81 individuals agreed to participate. Individuals underwent a baseline evaluation and then were randomly assigned to receive either N-acetyl cysteine (NAC) or placebo for seven days. Each subject was re-evaluated at 3 and 7 days. Outcome measures were the presence of the following sequelae of mTBI: dizziness, hearing loss, headache, memory loss, sleep disturbances, and neurocognitive dysfunction. The resolution of these symptoms seven days after the blast exposure was the main outcome measure in this study. Logistic regression on the outcome of 'no day 7 symptoms' indicated that NAC treatment was significantly better than placebo (OR = 3.6, p = 0.006). Secondary analysis revealed subjects receiving NAC within 24 hours of blast had an 86% chance of symptom resolution with no reported side effects versus 42% for those seen early who received placebo. This study, conducted in an active theatre of war, demonstrates that NAC, a safe pharmaceutical countermeasure, has beneficial effects on the severity and resolution of sequelae of blast induced mTBI. This is the first demonstration of an effective short term countermeasure for mTBI. Further work on long term outcomes and the potential use of NAC in civilian mTBI is warranted. ClinicalTrials.gov NCT00822263.

The author shares her expertise in tai chi, qigong, and medicine, emphasizing how tai chi and qigong aid in memory, emotional balance, and lifelong learning. This book features an illustrated manual detailing tai chi and qigong exercises to prevent brain aging; and concise, accessible guidance in combining elements of eastern and western medicine to form a new vision of brain health.--Publisher.

Cognitive sequelae often occur after acute carbon monoxide poisoning. This double-blind, randomized trial assigned subjects either to three sessions in a hyperbaric-oxygen chamber or to one normobaric-oxygen treatment plus two sessions of exposure to normobaric room air, all administered within 24 hours after the end of exposure to carbon monoxide. Cognitive sequelae six weeks later were less frequent among persons who received hyperbaric-oxygen therapy (25.0 percent) than among those who received normobaric-oxygen treatment (46.1 percent, P=0.007). Differences were sustained 12 months after the episode of acute carbon monoxide poisoning. The results of this double-blind trial support the use of hyperbaric oxygen. Carbon monoxide poisoning is a serious health problem 1 , 2 resulting in approximately 40,000 visits to the emergency department annually in the United States. 2 , 3 Unfavorable cognitive sequelae (problems with memory, attention or concentration, and affect) can occur immediately after exposure and persist or can be delayed, but they generally occur within 20 days after carbon monoxide poisoning. 1 – 6 Cognitive sequelae lasting one month 5 , 7 – 9 or more 2 , 4 appear to occur in 25 to 50 percent of patients with loss of consciousness or with carboxyhemoglobin levels greater than 25 percent. 2 , 7 , 8 The recommended treatment for acute carbon monoxide poisoning . . .

Background Alzheimer’s disease and related dementias (ADRD) are among the most feared age-related conditions. The aim of this study was to evaluate a brief psychological intervention to promote adaptive coping in older adults experiencing heightened fear of ADRD and investigate positive downstream effects on health-related secondary outcomes, including frequency of reported memory failures, psychosocial functioning, and quality of life. Methods Eighty-one older adults were recruited and randomized into REFRAME or active control intervention arms. Both groups received psycho-education and training in mindful monitoring of fears related to ADRD. The REFRAME group received an additional behavioral activation component intended to disrupt maladaptive avoidant coping (i.e., avoidance) strategies. Both groups completed 3-weeks of intervention exercises with accompanying questionnaires (baseline, mid- and post-intervention and 4-week follow-up). Results Adherence was strong (> 75%). We observed a significant reduction in ADRD-related fear and avoidance in both groups. Significant reductions were also observed for frequency of self-reported memory failures, anxiety, and depression. Depression was significantly reduced in the REFRAME group compared to the control group. Significant increases in participants’ ability to participate in social activities and well-being were also observed. Conclusions Findings suggest that a brief psychological intervention can mitigate ADRD-related fears and avoidant coping in older adults, and that benefits extend to broader health-related outcomes including anxiety, depression, social functioning, and well-being. Addressing ADRD-related fear has implications for healthy aging and risk reduction, as individuals may be more likely to engage in activities that are protective against ADRD but were previously avoided. Trial registration : https://clinicaltrials.gov/ct2/show/NCT04821960 .

Background Older adults’ cognitive abilities can be impaired through priming of negative age stereotypes. However, it is unclear whether the effects of negative priming can be extended to episodic memory, which is believed to be the most age-sensitive type among the long-term memory systems, in Asian populations. Social participation has recently emerged as a potential protective factor for maintaining the cognitive function of older adults. The purpose of this study was to examine the effects of negative age stereotype priming on episodic memory and the moderating role of social participation in the priming effect. Methods A total of 105 community-dwelling older adults residing in Hong Kong were randomly allocated to two experimental conditions. Participants were primed either with negative age stereotype words ( n  = 53) or neutral words ( n  = 52) using an implicit priming task. Episodic memory performance was assessed using the Hong Kong List Learning Task (HKLLT), which includes total learning, two delayed recalls and a recognition task. Analysis of covariance (ANCOVA) was used to assess group differences in the priming task and memory performance, while a series of moderation analyses were performed to examine the moderating effects of social participation. Results The group that received negative age stereotype priming performed significantly worse than the group that received neutral words in their episodic memory test. Additional analyses showed that socially active individuals might be less prone to the effects of negative age stereotypes for the recognition task only. Conclusions Older adults who are more socially active might be more immune to the effects of negative age stereotype priming on episodic memory. These results provide initial support for the hypothesis that social participation might act as an effective strategy to ward against negative age stereotype priming. Trial registration ClinicalTrials.gov: NCT04202120 (first posted December 17, 2019), (Retrospectively registered).