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Energetic Metabolism Impairment in Brain Dysfunction
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Energetic Metabolism Impairment in Brain Dysfunction

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Endocrinology & Metabolism".

Deadline for manuscript submissions: closed (31 October 2019) | Viewed by 9792

Special Issue Editors

Dr. Annamaria Cimini

E-Mail Website
Guest Editor
Department of Life, Health and Environmental Sciences, Università degli Studi dell'Aquila, L'Aquila, Italy
Interests: energetic metabolism; neurosciences; brain development; neurodegeneration
Special Issues, Collections and Topics in MDPI journals
Dr. Elisabetta Benedetti

E-Mail Website
Guest Editor
Department of Life, Health and Environmental Sciences, University of L’Aquila, L'Aquila, Italy
Interests: neurodegenerative disease; lipid metabolism; oxidative stress; PPARs
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Alterations in energetic metabolism and redox homeostasis are thought to be central components of neurodegeneration that result in the impairment of important homeostatic processes in neurons, such as protein quality control mechanisms, neurotransmitter release/metabolism, the axonal transport of vesicles, and cell survival. Importantly, both bioenergetics and redox homeostasis are coupled to neuro-glial energetic metabolism. Redox and metabolic homeostasis is carried out by a complex interaction between neurons, glia, and the extracellular microenvironment. Alterations of the neuronal environment and/or genetic mutations of key genes may result in different neurodegenerative conditions, i.e. Parkinson’s disease, Alzheimer’s disease, and Huntington’s disease. Moreover, energetic metabolism impairment may lead to neurotrophins depletion, resulting in the activation of death pathways and the downregulation of survival pathways.

In summary, the understanding of the complex mechanisms occurring during neurodegeneration, both as a consequence of the interaction of genetic background with the environment and as an alteration of neuron-glia crosstalk, may bring new insight into the complex scenarios of different neurodegenerative diseases and provide a basis for new therapeutic approaches.

Prof. Dr.  Annamaria Cimini
Prof. Dr. Elisabetta Benedetti
Guest Editors

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Keywords

  • Neurodegenerative diseases
  • Glucose metabolism
  • Lipid metabolism
  • Neurotrophins
  • Apoptosis
  • Mitochondria
  • Peroxisomes
  • Neurotransmitters

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Published Papers (2 papers)

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Research

19 pages, 2895 KiB  
Article
GSKIP-Mediated Anchoring Increases Phosphorylation of Tau by PKA but Not by GSK3beta via cAMP/PKA/GSKIP/GSK3/Tau Axis Signaling in Cerebrospinal Fluid and iPS Cells in Alzheimer Disease
by Huey-Jiun Ko, Shean-Jaw Chiou, Yu-Hui Wong, Yin-Hsuan Wang, Yun-Ling Lai, Chia-Hua Chou, Chihuei Wang, Joon-Khim Loh, Ann-Shung Lieu, Jiin-Tsuey Cheng, Yu-Te Lin, Pei-Jung Lu, Ming-Ji Fann, Chi-Ying Huang and Yi-Ren Hong
J. Clin. Med. 2019, 8(10), 1751; https://doi.org/10.3390/jcm8101751 - 21 Oct 2019
Cited by 20 | Viewed by 6620
Abstract
Based on the protein kinase A (PKA)/GSK3β interaction protein (GSKIP)/glycogen synthase kinase 3β (GSK3β) axis, we hypothesized that these might play a role in Tau phosphorylation. Here, we report that the phosphorylation of Tau Ser409 in SHSY5Y cells was increased by overexpression of [...] Read more.
Based on the protein kinase A (PKA)/GSK3β interaction protein (GSKIP)/glycogen synthase kinase 3β (GSK3β) axis, we hypothesized that these might play a role in Tau phosphorylation. Here, we report that the phosphorylation of Tau Ser409 in SHSY5Y cells was increased by overexpression of GSKIP WT more than by PKA- and GSK3β-binding defective mutants (V41/L45 and L130, respectively). We conducted in vitro assays of various kinase combinations to show that a combination of GSK3β with PKA but not Ca2+/calmodulin-dependent protein kinase II (CaMK II) might provide a conformational shelter to harbor Tau Ser409. Cerebrospinal fluid (CSF) was evaluated to extend the clinical significance of Tau phosphorylation status in Alzheimer’s disease (AD), neurological disorders (NAD), and mild cognitive impairment (MCI). We found higher levels of different PKA–Tau phosphorylation sites (Ser214, Ser262, and Ser409) in AD than in NAD, MCI, and normal groups. Moreover, we used the CRISPR/Cas9 system to produce amyloid precursor protein (APPWT/D678H) isogenic mutants. These results demonstrated an enhanced level of phosphorylation by PKA but not by the control. This study is the first to demonstrate a transient increase in phosphor-Tau caused by PKA, but not GSK3β, in the CSF and induced pluripotent stem cells (iPSCs) of AD, implying that both GSKIP and GSK3β function as anchoring proteins to strengthen the cAMP/PKA/Tau axis signaling during AD pathogenesis. Full article
(This article belongs to the Special Issue Energetic Metabolism Impairment in Brain Dysfunction)
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12 pages, 1614 KiB  
Article
Association between Achievement of Estimated Average Glucose Level and 6-Month Neurologic Outcome in Comatose Cardiac Arrest Survivors: A Propensity Score-Matched Analysis
by Yong Hun Jung, Byung Kook Lee, Kyung Woon Jeung, Dong Hun Lee, Hyoung Youn Lee, Yong Soo Cho, Chun Song Youn, Jung Soo Park and Yong II Min
J. Clin. Med. 2019, 8(9), 1480; https://doi.org/10.3390/jcm8091480 - 18 Sep 2019
Viewed by 2772
Abstract
We investigated whether achieving estimated average glucose (EAG) levels versus achieving standard glucose levels (180 mg/dL) was associated with neurologic outcome in cardiac arrest survivors. This single-center retrospective observational study included adult comatose cardiac arrest survivors undergoing therapeutic hypothermia (TH) from September 2011 [...] Read more.
We investigated whether achieving estimated average glucose (EAG) levels versus achieving standard glucose levels (180 mg/dL) was associated with neurologic outcome in cardiac arrest survivors. This single-center retrospective observational study included adult comatose cardiac arrest survivors undergoing therapeutic hypothermia (TH) from September 2011 to December 2017. EAG level was calculated using HbA1c obtained after the return of spontaneous circulation (ROSC), and the mean glucose level during TH was calculated. We designated patients to the EAG or standard glucose group according to whether the mean blood glucose level was closer to the EAG level or 180 mg/dL. Patients in the EAG and standard groups were propensity score- matched. The primary outcome was the 6-month neurologic outcome. The secondary outcomes were hypoglycemia (≤70 mg/dL) and serum neuron-specific enolase (NSE) at 48 h after ROSC. Of 384 included patients, 137 (35.7%) had a favorable neurologic outcome. The EAG group had a higher favorable neurologic outcome (104/248 versus 33/136), higher incidence of hypoglycemia (46/248 versus 11/136), and lower NSE level. After propensity score matching, both groups had similar favorable neurologic outcomes (24/93 versus 27/93) and NSE levels; the EAG group had a higher incidence of hypoglycemia (21/93 versus 6/93). Achieving EAG levels was associated with hypoglycemia but not neurologic outcome or serum NSE level. Full article
(This article belongs to the Special Issue Energetic Metabolism Impairment in Brain Dysfunction)
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