Neuroscience

Teach Me in 10

Science is a process, says Professor Yotam Ophir from the Department of Communication, University at Buffalo. This process is not finite. It involves a community of individuals coming together to continuously critique each other's research to further enhance, develop and update knowledge. In this Teach Me in 10, Professor Ophir explains the different narratives often used to communicate science and what impact these narratives can have on the general public's perception of scientific research. He also provides useful tips and tricks on how to communicate science effectively. You can read our recent interview published on Technology Networks [url][link]https://www.technologynetworks.com/tn/articles/scientific-storytelling-its-all-about-context-353303[/link][name]here[/name][/url]

How To Communicate Science Effectively With Professor Yotam Ophir

Aging

Aging-US published this trending research paper on September 21, 2020, entitled, “Alzheimer’s disease as a systems network disorder: chronic stress/dyshomeostasis, innate immunity, and genetics” by researchers from the Department of Neurology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA; Department of Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA; Buck Institute for Research on Aging, Novato, CA.

Abstract
Ineffective results of clinical trials of over 200 anti-Alzheimer's drug candidates, with a 99.6% attrition rate, suggest that the current paradigm of Alzheimer's disease (AD) may be incomplete, necessitating exploration of alternative and complementary frameworks.

Using algorithms for hypothesis independent search and expert-assisted synthesis of heterogeneous data, we attempted to reconcile multimodal clinical profiles of early-stage AD patients and accumulated research data within a parsimonious framework. Results of our analysis suggest that Alzheimer’s may not be a brain disease but a progressive system-level network disorder, which is driven by chronic network stress and dyshomeostasis. The latter can be caused by various endogenous and exogenous factors, such as chronic inflammatory conditions, infections, vascular dysfunction, head trauma, environmental toxicity, and immune disorders. Whether originating in the brain or on the periphery, chronic stress, toxicity, and inflammation are communicated to the central nervous system (CNS) via humoral and neural routes, preferentially targeting high-centrality regulatory nodes and circuits of the nervous system, and eventually manifesting as a neurodegenerative CNS disease.

In this report, we outline an alternative perspective on AD as a systems network disorder and discuss biochemical and genetic evidence suggesting the central role of chronic tissue injury/dyshomeostasis, innate immune reactivity, and inflammation in the etiopathobiology of Alzheimer’s disease.

Press release - https://www.aging-us.com/news_room/alzheimers-disease-as-a-systems-network-disorder

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DOI - https://doi.org/10.18632/aging.103883

Full text - https://www.aging-us.com/article/103883/text

Correspondence to: Alexei Kurakin email: akurakin@mednet.ucla.edu and Dale E. Bredesen email: dbredesen@mednet.ucla.edu

Keywords: Alzheimer’s disease, neurodegeneration, complex chronic disorder, network biology, systems biology

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at http://www.Aging-US.com​​ or connect with us on:

Twitter - https://twitter.com/AgingJrnl
Facebook - https://www.facebook.com/AgingUS/
SoundCloud - https://soundcloud.com/aging-us​
YouTube - https://www.youtube.com/agingus​
LinkedIn -  https://www.linkedin.com/company/aging​

Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls

Media Contact
18009220957
MEDIA@IMPACTJOURNALS.COM

Trending with Impact: Treating Alzheimer’s Disease as a Systems Network Disorder

In this week’s Teach Me in 10, we are joined by Dr. Sarah Rosen, a postdoctoral researcher in the Klein lab at the Washington University in St. Louis. Rosen discusses her recent efforts into discovering why the mosquito-borne West Nile Virus affects men more severely than women. She will outline why sex differences in a type of immune cell in the brain, called microglia, might underlie these different outcomes.

Why More Men Die From West Nile Virus With Dr. Sarah Rosen

Aging-US published this trending research paper on September 9, 2021, entitled, “Hyperbaric oxygen therapy alleviates vascular dysfunction and amyloid burden in an Alzheimer’s disease mouse model and in elderly patients” by researchers from the School of Neurobiology, Biochemistry and Biophysics, The George S. Wise Faculty of Life Sciences, Tel Aviv University, Tel-Aviv, Israel; Sagol School of Neuroscience, Tel Aviv University, Tel-Aviv, Israel; Sackler School of Medicine, Tel Aviv University, Tel-Aviv, Israel; Sagol Center for Hyperbaric Medicine and Research, Assaf Harofeh Medical Center, Be’er Ya’akov, Israel.

Abstract
Vascular dysfunction is entwined with aging and in the pathogenesis of Alzheimer’s disease (AD) and contributes to reduced cerebral blood flow (CBF) and consequently, hypoxia. Hyperbaric oxygen therapy (HBOT) is in clinical use for a wide range of medical conditions. In the current study, we exposed 5XFAD mice, a well-studied AD model that presents impaired cognitive abilities, to HBOT and then investigated the therapeutical effects using two-photon live animal imaging, behavioral tasks, and biochemical and histological analysis. HBOT increased arteriolar luminal diameter and elevated CBF, thus contributing to reduced hypoxia. Furthermore, HBOT reduced amyloid burden by reducing the volume of pre-existing plaques and attenuating the formation of new ones. This was associated with changes in amyloid precursor protein processing, elevated degradation and clearance of Aß protein and improved behavior of 5XFAD mice. Hence, our findings are consistent with the effects of HBOT being mediated partially through a persistent structural change in blood vessels that reduces brain hypoxia. Motivated by these findings, we exposed elderly patients with significant memory loss at baseline to HBOT and observed an increase in CBF and improvement in cognitive performances. This study demonstrates HBOT efficacy in hypoxia-related neurological conditions, particularly in AD and aging.

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DOI - https://doi.org/10.18632/aging.203485

Full text - https://www.aging-us.com/article/203485/text

Correspondence to: Uri Ashery email: uria@tauex.tau.ac.il

Keywords: Alzheimer's disease, hyperbaric oxygen therapy, vascular dysfunction, cerebral blood flow, amyloid burden, aging

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at http://www.Aging-US.com​​ or connect with us on:

Twitter - https://twitter.com/AgingJrnl
Facebook - https://www.facebook.com/AgingUS/
SoundCloud - https://soundcloud.com/aging-us​
YouTube - https://www.youtube.com/agingus​
LinkedIn -  https://www.linkedin.com/company/aging​

Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls

Media Contact
18009220957
MEDIA@IMPACTJOURNALS.COM

Trending with Impact: Hyperbaric Oxygen Therapy Alleviates Vascular Dysfunction and Amyloid Burden

Aging-US published this high-scoring research paper on August 15, 2019, entitled, “Rejuvenation of brain, liver and muscle by simultaneous pharmacological modulation of two signaling determinants, that change in opposite directions with age,” by researchers from the Department of Bioengineering and QB3 Institute, University of California, Berkeley, Berkeley, CA; Department of Molecular, Cell and Developmental Biology, University of California, Santa Cruz, Santa Cruz, CA.

Abstract:
We hypothesize that altered intensities of a few morphogenic pathways account for most/all the phenotypes of aging. Investigating this has revealed a novel approach to rejuvenate multiple mammalian tissues by defined pharmacology. Specifically, we pursued the simultaneous youthful in vivo calibration of two determinants: TGF-beta which activates ALK5/pSmad 2,3 and goes up with age, and oxytocin (OT) which activates MAPK and diminishes with age. The dose of Alk5 inhibitor (Alk5i) was reduced by 10-fold and the duration of treatment was shortened (to minimize overt skewing of cell-signaling pathways), yet the positive outcomes were broadened, as compared with our previous studies. Alk5i plus OT quickly and robustly enhanced neurogenesis, reduced neuro-inflammation, improved cognitive performance, and rejuvenated livers and muscle in old mice. Interestingly, the combination also diminished the numbers of cells that express the CDK inhibitor and marker of senescence p16 in vivo. Summarily, simultaneously re-normalizing two pathways that change with age in opposite ways (up vs. down) synergistically reverses multiple symptoms of aging.

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DOI - https://doi.org/10.18632/aging.102148

Full text - https://www.aging-us.com/article/102148/text

Correspondence to: Irina M. Conboy email: iconboy@berkeley.edu

Keywords: muscle repair, TGF-beta, oxytocin, neurogenesis, neuro-inflammation, cognition, liver health

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at http://www.Aging-US.com​​ or connect with us on:

Twitter - https://twitter.com/AgingJrnl​
Facebook - https://www.facebook.com/AgingUS/​
SoundCloud - https://soundcloud.com/aging-us​
YouTube - https://www.youtube.com/agingus​
LinkedIn -  https://www.linkedin.com/company/aging​

Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls

Media Contact
18009220957
MEDIA@IMPACTJOURNALS.COM

Top-Performer: TGF-beta and Oxytocin Reversed to Reverse Aging

Aging-US published this trending high-scoring research paper back on June 12, 2016, entitled, “Reversal of cognitive decline in Alzheimer's disease,” by researchers from the University of California, Los Angeles, CA; Buck Institute for Research on Aging, Novato, CA; California Pacific Medical Center, San Francisco, CA; Private Practice of Psychiatry, Tucson, AZ; Brainreader, Horsens, Denmark.


Abstract:
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.

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DOI - https://doi.org/10.18632/aging.100981
Full text - https://www.aging-us.com/article/100981/text

Correspondence to: Dale E. Bredesen, MD email: dbredesen@buckinstitute.org

Keywords: neurodegeneration, cognition, biomarkers, dementia, neuropsychology, imaging, Alzheimer's disease, Apolipoprotein E

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at http://www.Aging-US.com​​ or connect with us on:

Twitter - https://twitter.com/AgingJrnl​
Facebook - https://www.facebook.com/AgingUS/​
SoundCloud - https://soundcloud.com/aging-us​
YouTube - https://www.youtube.com/agingus​
LinkedIn -  https://www.linkedin.com/company/aging​

Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls

Media Contact
18009220957
MEDIA@IMPACTJOURNALS.COM

Top-Performer: Reversal of Cognitive Decline in Alzheimer's Disease

Aging-US published this trending editorial on July 12, 2021, entitled, “Inhibition of heat shock proteins increases autophagosome formation, and reduces the expression of APP, Tau, SOD1 G93A and TDP-43” by researchers from the Department of Biochemistry and Molecular Biology, Richmond, VA; Department of Pharmacology and Toxicology, Richmond, VA; Department of Medicine, Virginia Commonwealth University, Richmond, VA; Translational Genomics Research Institute (TGEN), Phoenix, AZ; Banner Alzheimer’s Institute, Phoenix, AZ.

Abstract
Aberrant expression and denaturation of Tau, amyloid-beta and TDP-43 can lead to cell death and is a major component of pathologies such as Alzheimer’s Disease (AD). AD neurons exhibit a reduced ability to form autophagosomes and degrade proteins via autophagy. Using genetically manipulated colon cancer cells we determined whether drugs that directly inhibit the chaperone ATPase activity or cause chaperone degradation and endoplasmic reticulum stress signaling leading to macroautophagy could reduce the levels of these proteins. The antiviral chaperone ATPase inhibitor AR12 reduced the ATPase activities and total expression of GRP78, HSP90, and HSP70, and of Tau, Tau 301L, APP, APP692, APP715, SOD1 G93A and TDP-43. In parallel, it increased the phosphorylation of ATG13 S318 and eIF2A S51 and caused eIF2A-dependent autophagosome formation and autophagic flux. Knock down of Beclin1 or ATG5 prevented chaperone, APP and Tau degradation. Neratinib, used to treat HER2+ breast cancer, reduced chaperone levels and expression of Tau and APP via macroautophagy, and neratinib interacted with AR12 to cause further reductions in protein levels. The autophagy-regulatory protein ATG16L1 is expressed as two isoforms, T300 or A300: Africans trend to express T300 and Europeans A300. We observed higher basal expression of Tau in T300 cells when compared to isogenic A300 cells. ATG16L1 isoform expression did not alter basal levels of HSP90, HSP70 or HSP27, however, basal levels of GRP78 were reduced in A300 cells. The abilities of both AR12 and neratinib to stimulate ATG13 S318 and eIF2A S51 phosphorylation and autophagic flux was also reduced in A300 cells. Our data support further evaluation of AR12 and neratinib in neuronal cells as repurposed treatments for AD.

Sign up for free Altmetric alerts about this article - https://oncotarget.altmetric.com/details/email_updates?id=10.18632%2Foncotarget.203297

DOI - https://doi.org/10.18632/aging.203297

Full text - https://www.aging-us.com/article/203297/text

Correspondence to: Paul Dent email: paul.dent@vcuhealth.org
 
Keywords: Alzheimer's, chaperone, GRP78, autophagy, neratinib

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

Please visit our website at http://www.Aging-US.com​​ or connect with us on:

Twitter - https://twitter.com/AgingJrnl​
Facebook - https://www.facebook.com/AgingUS/​
SoundCloud - https://soundcloud.com/aging-us​
YouTube - https://www.youtube.com/agingus​
LinkedIn -  https://www.linkedin.com/company/aging​

Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls

Media Contact
18009220957
MEDIA@IMPACTJOURNALS.COM

Trending with Impact: Knockdown of Disease Specific Proteins APP, Tau, SOD1 G93A and TDP-43

Analytical Cannabis 

Speaking at the Analytical Cannabis Expo East Online 2021 back in October, Dr. Staci Gruber, Associate Professor of Psychiatry at Harvard Medical School presented the clinical trial results from a full-spectrum cannabidiol (CBD) sublingual product for anxiety.

Abstract: In this talk, Dr. Gruber will discuss her groundbreaking clinical trial of a full-spectrum cannabidiol (CBD) sublingual product for anxiety. She will describe the path from product selection to implementation of the clinical trial, including legal considerations, a summary of formulation procedures, and an overview of laboratory analyses (e.g., cannabinoid quantification and product safety tests). She will describe the study design which includes the recently completed four-week open-label phase as well as a currently in-progress double-blind phase designed to assess the efficacy of a full spectrum CBD product vs a matched CBD isolate vs placebo. Dr. Gruber will also highlight promising results from the open-label phase, which noted significant reductions in anxiety and related symptomatology over the course of treatment. In addition, she will describe the impact of four weeks of CBD treatment on aspects of cognitive functioning, including executive function and memory. Finally, she will present interesting findings from the clinical trial regarding urinary THC status, which have important public health implications.

Formulating the Case for Cannabidiol: Methods and results from an open-label anxiety trial

Speaking at the Analytical Cannabis Expo East Online 2021 back in October, Dr. Andrew Rosenstein, CEO at Steep Hill and Medical Director and Lead GI Physicianat St. Joseph's Medical Center Staci Gruber, Associate Professor of Psychiatry at Harvard Medical School presented the reason why cannabis testing is crucial from an MD’s perspective.

Abstract: A lot can go wrong with food or cannabis, which can result in serious complications for users, such as heavy metal toxicity and bacteria-food borne illness. Testing is therefore necessary as it protects patients, consumers and can encourage people to exit the illicit, unregulated market. Although most products are safe, compliance and oversight are key to protect our industry and critical for future public acceptance. This presentation will cover the reasons why testing is critical from an MD’s perspective, important cannabis testing parameters, medical complications which can result from testing negligence, and global standards for cannabis testing.

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