Memory Cure: How to Protect Your Brain Against Memory Loss and Alzheimers Disease 2004 Edition


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Treatment effects of therapeutic cholinesterase inhibitors on visuospatial processing in Alzheimer's disease: a longitudinal functional MRI study. Dement Geriatr Cogn Disord. Prolonged cholinergic enrichment influences regional cortical activation in early Alzheimer's disease. Neuropsychiatr Dis Treat. Regional brain activity after prolonged cholinergic enhancement in early Alzheimer's disease.

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Magn Reson Imaging. Established donepezil treatment modulates task relevant regional brain activation in early Alzheimer's disease. Responders to ChEI treatment of Alzheimer's disease show restitution of normal regional cortical activation. Inhibition of hippocampal function in mild cognitive impairment: targeting the cholinergic hypothesis. Challenging the cholinergic system in mild cognitive impairment: a pharmacological fMRI study.

Response of the medial temporal lobe network in amnestic mild cognitive impairment to therapeutic intervention assessed by fMRI and memory task performance.


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Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study. Correspondence to Federica Agosta. ES declares that she has no competing interests. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Reprints and Permissions. Search all BMC articles Search. Abstract Background A growing number of pharmacological and nonpharmacological trials have been performed to test the efficacy of approved or experimental treatments in Alzheimer disease AD and mild cognitive impairment MCI.

Main body This critical review aimed to identify and discuss the available studies that have tested the efficacy of pharmacological and nonpharmacological treatments in AD and MCI cases using task-based or resting-state fMRI measures as primary outcomes. Methods Formal literature review research A formal literature review was conducted on Medline in two separate sections, one for pharmacological and the other for nonpharmacological studies. Results Pharmacological studies We obtained articles.

Full size image. Discussion Patient selection, randomization, and allocation The definition of the clinical population is a very critical point. Type, intensity, and duration of treatment The persistence of effects, along with generalization of gain in everyday life, is the critical point of pharmacological and nonpharmacological therapies. The choice of outcome measures The main difficulty for these studies is to transfer outcome measures from the laboratory to real life. Incomplete outcomes, drop-out cases, and sample size Incomplete outcome measures are often an important problem in these studies.

Conclusions This critical review pointed at both strengths and caveats of the existing literature on the effects of pharmacological and nonpharmacological treatments on brain fMRI in AD and MCI. References 1. Article PubMed Google Scholar 3. Article PubMed Google Scholar 7. Article PubMed Google Scholar 9. Article PubMed Google Scholar Google Scholar PubMed Google Scholar Article Google Scholar Acknowledgements Not applicable. Funding None. Availability of data and materials Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.

You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. Help us improve our products. Sign up to take part. A Nature Research Journal. Proteinopathies constitute a group of diseases in which certain proteins are abnormally folded leading to aggregation and eventual cell failure. Hence, we genetically engineered a molecular chaperone that was selectively delivered to this cellular location.

Proteinopathies, also known as protein misfolding disorders, are neurodegenerative disorders characterized by an initial self-association of misfolded proteins that eventually aggregate into toxic assemblies. Early in vitro studies are consistent with a regulatory role of chaperones in protein misfolding and aggregation 2. Molecular chaperones are responsible for the proper folding and maturation of nascent proteins as well as the re-folding or degradation of misfolded ones.

A large number of these chaperones are heat shock proteins Hsps. These proteins were initially characterized for their response to heat shock stress, which is mostly regulated by gene expression via the heat shock factor 1 Hsf1. Hsps trigger efficient responses against cellular stress 3. Molecular chaperones can be found intracellularly i. Functionally, Hsp70 display two domains, the substrate binding domain SBD , which recognizes specific substrates or client proteins, and the nucleotide binding domain NBD , which binds ATP and regulates client association through ATP hydrolysis.

Whether Hsp70 is located extracellularly is not clear, but some reports claim both intracellular and extracellular roles for Hsp70 3 , 6 , 7. AD is the most prevalent neurodegenerative disorder; a dementia that particularly affects the aging population with a profound personal, medical and social impact. These kinases eventually hyperphosphorylate tau, which has been proposed to be the executor of the pathogenic process, affecting synaptic function and leading to cognitive impairments.

Interestingly, ubiquitous expression of tau selectively affected the mushroom body MB neurons, which is consistent with the neuron-specific pathology of AD 14 , In recent years, Drosophila models of cognition have been established as a standard system to explore the learning and memory mechanisms at the molecular, cellular, and behavioral levels.

The Memory Cure: How to Protect Your Brain Against Memory Loss and Alzheimer's Disease

Studies in the past 3 decades has unraveled important parallelisms between Drosophila and mammals concerning the anatomy of the olfactory pathway, the organization of neuronal circuits and the signaling cascades underlying the formation of memories The Drosophila MBs are a bilateral structure located in the dorsal region of the brain and comprised of approximately two thousand neurons in each brain hemisphere, the Kenyon Cells.

The axons of these neurons project ventrally to form the MB lobes, where they connect with a plethora of post-synaptic neurons through the release of acetylcholine. The neuronal activity that Kenyon cells orchestrate plays a major role in the formation and storage of olfactory memories 21 , 22 , The MB neurons in combination with the use of olfactory classical conditioning protocols are ideally suited to examine the effectiveness of novel therapeutic agents targeting the neurodegenerative actions of human amyloids, their efficiency, and functionality.

As these amyloids are mostly secreted to the extracellular space, we engineered a molecular system that delivers a potential blocking agent, the Hsp70, to this extracellular region. In that study, we monitored locomotor activity as the alternative physiological assay to evaluate neuronal activity. Although this method resulted effective in providing functional evidence, the paradigm was not relevant in the context of AD.

Our fly model displayed severe memory impairments after olfactory classical conditioning Decreases in temperature from this optimal value reduce the level of Gal4 and, consequently, the transcriptional activity of the Gal4 over the UAS construct. In control flies, memory performance was statistically comparable at both temperatures Supplementary Fig.

By day 30, memory performance was drastically disrupted and at comparable levels irrespective of the temperature. Flies were tested immediately after conditioning. Memory performance index P. Remarkably, the memory impairments were present i. Frontal i and dorsal ii view of the MB lobes and dorsal iii and frontal iv view of the MB calyxes.

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No significant defects were found at the macroscopic level. Otherwise, memory deficits would be the result of a disrupted perception rather than a deficiency in the formation of memories per se. Thus, it was critical to exclude the possibility that these memory impairments were the result of abnormalities in stimuli perception. At day 15, however, shock and odor perception was identical to controls. The Hsp70 is a molecular chaperone with demonstrated neuroprotective activity against intracellular amyloids that can also tackle extracellular targets through genetic engineering Further, memory acquisition of one- Fig.

This protective effect was observed for both isoforms, the Hsp70 delivered to the extracellular matrix as well as the one delivered to the cytosol and, in some cases, memory performance of flies expressing the Hsp70 tended to be higher than that of control flies. Interestingly, Thirty-day-old flies did not show any sign of memory improvement when compare with their respective control group non-expressing secHsp Again, the intracellular function of Hsp70 did not halt the progression of memory loss related to aging.

Cytosolic and secreted forms of Hsp70 do not enhance memory performance in young or elder flies. Flies were trained at days 1 a , 5 b , 15 c or 30 d post-eclosion using olfactory classical conditioning and then tested immediately after training. Despite the tremendous advance experienced in the understanding of the AD pathogenesis, this knowledge has been sterile in developing therapies that efficiently reduce the symptoms of the disease.

Remarkably, regardless of the severity observed for these memory deficits, we discovered that co-expression of the chaperone Hsp70 reverted the cognitive impairments to levels equivalent to those of control animals, supporting a potential application of this family of chaperones for palliative treatments of AD. Based on these observations, it is possible to be facing two independent mechanisms of action for Hsp70, an intracellular clearance pathway 6 and an extracellular masking effect On the one hand, Hsp70 exhibits a variety of functions in the extracellular space.

This machinery is responsible for activating stress responses. Therefore, cytosolic Hsp70 could also mediate its protective effect on memory loss through its holdase activity, a process that we previously postulated under the masking hypothesis Hsp70 has also been involved in the regulation of macromolecular complexes and the control of protein-protein interactions 3.

Additionally, Hsp70 exerts a pleiotropic effect against cellular stress. The role of Hsp70 preventing oxidative stress, mitochondrial depolarization and cell death has been previously reported The ability to independently manipulate intracellular and extracellular Hsp70s enabled discrimination of the differential effects that each of these molecular cascades exert on the various symptoms of AD.

The cytosolic form seems to protect specifically against cell death and the synaptic effects underlying the loss of memory 6 as we also show here. Our brains need physical and social activities to stay healthy. Aug 31, Meredith rated it it was amazing. I loved the book. I liked the narrator audible book and I got a lot of information about the brain, memory, and how to protect against early onset dementia. I my age I like to hear these things! This book reminded me of a Dale Carnegie book. I think the narrator was the same. My philosophy in life is that many things we do are self-fulfilling prophecies.

People create their own realities in their head.


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I believe it applies with Alzheimer's disease Old Timer's Disease , in that it can be preventable through living the basics - exercise, good social interaction, and learning to stimulate the mind AND positive thinking. I want to see some studies with Alzheimer's disease increasing over t This book reminded me of a Dale Carnegie book. Many people think they have memory problems when in reality they don't.

It's because they don't try at all to remember crap and put their mind on cruise control by watching TV. And in the famous words of Yoda "that is why you fail. When I go and see her I tell her that her memory is getting better and to not believe everyone else that tells her it's getting worse or that she's forgetting things. It's working. I liked the little tecnicas at the end to help with remember dinghies.

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View 2 comments. I found this book through my husband at a time when I was working on an Alzheimer's Study. I often reccommended it to the caretakers of our patients and other friends. Crucial to good brain health is working those brain cells all of the time with new projects and new problems and solutions. Also, physical health and activity are important.

Jul 26, Mark rated it liked it. This book keeps things positive. Fotuhi reminds us that Alzheimer's is a rare disease, that we likely don't have it, especially if we're young, and that we can make choices to lower the risk of Alzheimer's in our future. He is a big proponent of exercise, healthy diet, and supplements, specifically Vitamins E and C. This is a helpful, quick book for people who are experiencing anxiety because of memory lapses. May 30, Dolly rated it really liked it Shelves: non-fiction. Apr 25, T. Zalecki rated it liked it. I purchased this book to alleviate my fears of having Alzheimer's And it was also very informative in terms of how memory works in the brain and things you can do to improve your memory

Memory Cure: How to Protect Your Brain Against Memory Loss and Alzheimers Disease 2004 Edition Memory Cure: How to Protect Your Brain Against Memory Loss and Alzheimers Disease 2004 Edition
Memory Cure: How to Protect Your Brain Against Memory Loss and Alzheimers Disease 2004 Edition Memory Cure: How to Protect Your Brain Against Memory Loss and Alzheimers Disease 2004 Edition
Memory Cure: How to Protect Your Brain Against Memory Loss and Alzheimers Disease 2004 Edition Memory Cure: How to Protect Your Brain Against Memory Loss and Alzheimers Disease 2004 Edition
Memory Cure: How to Protect Your Brain Against Memory Loss and Alzheimers Disease 2004 Edition Memory Cure: How to Protect Your Brain Against Memory Loss and Alzheimers Disease 2004 Edition
Memory Cure: How to Protect Your Brain Against Memory Loss and Alzheimers Disease 2004 Edition Memory Cure: How to Protect Your Brain Against Memory Loss and Alzheimers Disease 2004 Edition
Memory Cure: How to Protect Your Brain Against Memory Loss and Alzheimers Disease 2004 Edition Memory Cure: How to Protect Your Brain Against Memory Loss and Alzheimers Disease 2004 Edition
Memory Cure: How to Protect Your Brain Against Memory Loss and Alzheimers Disease 2004 Edition Memory Cure: How to Protect Your Brain Against Memory Loss and Alzheimers Disease 2004 Edition

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