Alzheimers

2019 RYB ALZ Risk - Main Opt-In.

This is the first time a randomized, double-blind, clinical trial has shown that a nutritional intervention can help to conserve the ability of prodromal AD patients to carry out everyday tasks, such as paying bills, or finding your way around, as measured by the Clinical Dementia Rating-Sum of Boxes (CDR-SB) -- a combined measure for the ability to think and perform everyday tasks. This is important because those with prodromal AD currently have no approved, available pharmacological options.

The disaccharide trehalose is commonly considered to stimulate autophagy. Cell treatment with trehalose could decrease cytosolic aggregates of potentially pathogenic proteins, including mutant huntingtin, α-synuclein, and phosphorylated tau that are associated with neurodegenerative diseases. Here, …

In our discussions in recent years about Alzheimer's disease, certainly one dietary recommendation seems to gain the spotlight and that is a diet that helps produce ketones. To be fair, most of the support for a ketogenic diet thus far has been theoretical although early animal research has been supportive. Now, I'm excited to report that an actual interventional trial using the ketogenic diet in Alzheimer's patients has been completed and has demonstrated quite remarkable results. The study, performed by my friend Dr. Matthew Phillips in New Zealand, demonstrated significant improvement in a variety of parameters in Alzheimer's patients who were placed on a ketogenic diet in comparison to their standard diet. Here is the actual study: https://www.drperlmutter.com/study/randomized-crossover-trial-of-a-modified-ketogenic-diet-in-alzheimers-disease/ https://www.drperlmutter.com/ketogenic-diet-proves-effective-in-alzheimers-disease/ Many of you may remember Dr. Phillips as he appeared on the podcast in the past describing his results of using a ketogenic diet, successfully, in Parkinson's disease: https://www.drperlmutter.com/the-empowering-neurologist-with-dr-matthew-phillips/ Here's more information about him. ==== Matt is a full-time clinical and research neurologist at Waikato Hospital, Hamilton, New Zealand. His foremost passion is to explore the potential feasibility, safety, and efficacy of metabolic therapies, particularly fasting and ketogenic diets, in creating alternate metabolic states that may improve not only the symptoms, but also function and quality of life, for people with a variety of difficult disorders. ___________________________ Instagram: https://www.instagram.com/davidperlmutter/ Website: https://www.drperlmutter.com/ Subscribe to our channel: https://www.youtube.com/channel/UCDRl_UAXxbHyOOjklnA0dxQ/?sub_confirmation=1

During the last years, epigenetic processes have emerged as important factors for many neurodegenerative diseases, such as Alzheimer’s disease (AD). These complex diseases seem to have a heritable component; however, genome-wide association studies failed to identify the genetic loci involved in the etiology. So, how can these changes be transmitted from one generation to the next? Answering this question would allow us to understand how the environment can affect human populations for multiple generations and explain the high prevalence of neurodegenerative diseases, such as AD. This review pays particular attention to the relationship among epigenetics, cognition, and neurodegeneration across generations, deepening the understanding of the relevance of heritability in neurodegenerative diseases. We highlight some recent examples of EI induced by experiences, focusing on their contribution of processes in learning and memory to point out new targets for therapeutic interventions. Here, we first describe the prominent role of epigenetic factors in memory processing. Then, we briefly discuss aspects of EI. Additionally, we summarize evidence of how epigenetic marks inherited by experience and/or environmental stimuli contribute to cognitive status offspring since better knowledge of EI can provide clues in the appearance and development of age-related cognitive decline and AD.

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In Alzheimer’s disease (AD), amyloid-β (Aβ) oligomers are considered key mediators of synaptic dysfunction and cognitive impairment. These unstable intermediate Aβ species can interfere with different cellular organelles, leading to neuronal cell death, through the formation of Ca2+-permeable membrane pores, impairment in the levels of acetylcholine neurotransmitters, increased insulin resistance, promotion of pro-inflammatory cascades, among others. Based on a series of evidences that indicate the key role of glycosaminoglycans (GAGs) in amyloid plaque formation, we evaluated the capacity of four monosaccharides, i.e., glucosamine (GlcN), N-acetyl glucosamine (GlcNAc), glucosamine-6-sulfate (GlcN6S), and glucosamine-6-phosphate (GlcN6P), to reduce the Aβ-mediated pathological hallmarks. The tested monosaccharides, in particular, GlcN6S and GlcN6P, were able to interact with Aβ aggregates, reducing neuronal cell death, Aβ-mediated damage to the cellular membrane, acetylcholinesterase activity, insulin resistance, and pro-inflammation levels.