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Biomedicines
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10th Anniversary of Biomedicines—Molecular Mechanisms and Treatments on Neurodegenerative...
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10th Anniversary of Biomedicines—Molecular Mechanisms and Treatments on Neurodegenerative Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (15 November 2022) | Viewed by 13011

Special Issue Editor

Prof. Dr. Kuen-Jer Tsai

E-Mail Website
Guest Editor
Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan 704, Taiwan
Interests: neurodegenerative diseases; dementia; Alzheimer's disease; frontotemporal lobe degeneration; stroke; drugs and treatments on brain diseases; stem cell therapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The year 2023 marks the 10th anniversary of Biomedicines, a peer-reviewed open access journal in the biomedical field. So far, Biomedicines has published more than 2700 papers from more than 17,000 authors. We appreciate each author, reviewer, and academic editor whose support has brought us to where we are today.

To celebrate this significant milestone, we aim to publish a Special Issue entitled 10th Anniversary of Biomedicines—Molecular Mechanisms and Treatments on Neurodegenerative Diseases. Degeneration and death of neurons is the fundamental process responsible for the clinical manifestations of many different neurological disorders of aging. Age-related neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), stroke, and frontotemporal lobar dementia are highly associated with the increase in lifespan and display behavioral deficits in memory, cognition, problem solving, executive function, language, emotion, and related brain functions. At present, more than 25 million people in the world are affected by dementia, and by 2050, new cases of dementia are expected to result in nearly 1 million new cases per year. Recent studies have indicated that the most promising treatment strategy targeting the abnormal protein aggregation can reverse the pathogenesis of neurodegenerative diseases. However, the underlying mechanisms associated with neurodegeneration are not fully understood, and the efficacy of current treatments for neurodegenerative diseases are still limited. Causative factors for neurodegeneration have yet to be fully clarified. This Special Issue of Biomedicines attempts to investigate the novel mechanism involved in neurodegenerative disease models and further develop novel therapeutic strategies. Original articles and reviews are welcome for publication on the topic.

Prof. Dr. Kuen-Jer Tsai
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • neurodegeneration
  • neurodegenerative diseases
  • dementia
  • Alzheimer's disease
  • Parkinson's disease
  • frontotemporal lobar degeneration
  • stroke brain injury
  • neurogenesis
  • neuroinflammation
  • autophagy
  • physical treatment
  • drug treatment
  • cell therapy

Related Special Issue

Published Papers (5 papers)

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Research

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16 pages, 4368 KiB  
Article
Minocycline Inhibits Microglial Activation and Improves Visual Function in a Chronic Model of Age-Related Retinal Degeneration
by Xuan Du, Eimear M. Byrne, Mei Chen and Heping Xu
Biomedicines 2022, 10(12), 3222; https://doi.org/10.3390/biomedicines10123222 - 12 Dec 2022
Cited by 1 | Viewed by 1733
Abstract
Age-related macular degeneration (AMD) is a chronic disease, which progresses slowly from early to late stages over many years. Inflammation critically contributes to the pathogenesis of AMD. Here, we investigated the therapeutic potential of minocycline in a chronic model of AMD (i.e., the [...] Read more.
Age-related macular degeneration (AMD) is a chronic disease, which progresses slowly from early to late stages over many years. Inflammation critically contributes to the pathogenesis of AMD. Here, we investigated the therapeutic potential of minocycline in a chronic model of AMD (i.e., the LysMCre-Socs3fl/flCx3cr1gfp/gfp double knockout [DKO] mice). Five-month-old DKO and wild type (WT) (Socs3fl/fl) mice were gavage fed with minocycline (25 mg/kg daily) or vehicle (distilled water) for 3 months. At the end of the treatment, visual function and retinal changes were examined clinically (using electroretinography, fundus photograph and optic coherence tomography) and immunohistologically. Three months of minocycline treatment did not affect the body weight, behaviour and general health of WT and DKO mice. Minocycline treatment enhanced the a-/b-wave aptitudes and increased retinal thickness in both WT and DKO. DKO mouse retina expressed higher levels of Il1b, CD68 and CD86 and had mild microglial activation, and decreased numbers of arrestin+ photoreceptors, PKCα+ and secretagogin+ bipolar cells compared to WT mouse retina. Minocycline treatment reduced microglial activation and rescued retinal neuronal loss in DKO mice. Our results suggest that long-term minocycline treatment is safe and effective in controlling microglial activation and preserving visual function in chronic models of AMD. Full article
(This article belongs to the Special Issue 10th Anniversary of Biomedicines—Molecular Mechanisms and Treatments on Neurodegenerative Diseases)
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19 pages, 9326 KiB  
Article
Retinal Circular RNA hsa_circ_0087207 Expression Promotes Apoptotic Cell Death in Induced Pluripotent Stem Cell-Derived Leber’s Hereditary Optic Neuropathy-like Models
by Yi-Ping Yang, Yuh-Lih Chang, Yun-Hsien Lai, Ping-Hsing Tsai, Yu-Jer Hsiao, Long Hoang Nguyen, Xue-Zhen Lim, Chang-Chi Weng, Yu-Ling Ko, Chang-Hao Yang, De-Kuang Hwang, Shih-Jen Chen, Shih-Hwa Chiou, Guang-Yuh Chiou, An-Guor Wang and Yueh Chien
Biomedicines 2022, 10(4), 788; https://doi.org/10.3390/biomedicines10040788 - 28 Mar 2022
Cited by 4 | Viewed by 2139
Abstract
Backgrounds: Leber’s hereditary optic neuropathy (LHON) is known as an inherited retinal disorder characterized by the bilateral central vision loss and degeneration of retinal ganglion cells (RGCs). Unaffected LHON carriers are generally asymptomatic, suggesting that certain factors may contribute to the disease [...] Read more.
Backgrounds: Leber’s hereditary optic neuropathy (LHON) is known as an inherited retinal disorder characterized by the bilateral central vision loss and degeneration of retinal ganglion cells (RGCs). Unaffected LHON carriers are generally asymptomatic, suggesting that certain factors may contribute to the disease manifestations between carriers and patients who carry the same mutated genotypes. Methods: We first aimed to establish the iPSC-differentiated RGCs from the normal healthy subject, the carrier, and the LHON patient and then compared the differential expression profile of circular RNAs (CircRNAs) among RGCs from these donors in vitro. We further overexpressed or knocked down the most upregulated circRNA to examine whether this circRNA contributes to the distinct phenotypic manifestations between the carrier- and patient-derived RGCs. Results: iPSCs were generated from the peripheral blood cells from the healthy subject, the carrier, and the LHON patient and successfully differentiated into RGCs. These RGCs carried equivalent intracellular reactive oxygen species, but only LHON-patient iPSC-derived RGCs exhibited remarkable apoptosis. Next-generation sequencing and quantitative real-time PCR revealed the circRNA hsa_circ_0087207 as the most upregulated circRNA in LHON-patient iPSC-derived RGCs. Overexpression of hsa_circ_0087207 increased the apoptosis in carrier iPSC-derived RGCs, while knockdown of hsa_circ_0087207 attenuated the apoptosis in LHON-patient iPSC-derived RGCs. Predicted by bioinformatics approaches, hsa_circ_0087207 acts as the sponge of miR-665 to induce the expression of a variety of apoptosis-related genes in LHON patient iPSC-derived RGCs. Conclusions: Our data indicated that hsa_circ_0087207 upregulation distinguishes the disease phenotype manifestations between iPSC-derived RGCs generated from the LHON patient and carrier. Targeting the hsa_circ_0087207/miR-665 axis might hold therapeutic promises for the treatment of LHON. Full article
(This article belongs to the Special Issue 10th Anniversary of Biomedicines—Molecular Mechanisms and Treatments on Neurodegenerative Diseases)
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Review

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24 pages, 3679 KiB  
Review
Why Is Iron Deficiency/Anemia Linked to Alzheimer’s Disease and Its Comorbidities, and How Is It Prevented?
by Karin Fehsel
Biomedicines 2023, 11(9), 2421; https://doi.org/10.3390/biomedicines11092421 - 30 Aug 2023
Cited by 1 | Viewed by 3162
Abstract
Impaired iron metabolism has been increasingly observed in many diseases, but a deeper, mechanistic understanding of the cellular impact of altered iron metabolism is still lacking. In addition, deficits in neuronal energy metabolism due to reduced glucose import were described for Alzheimer’s disease [...] Read more.
Impaired iron metabolism has been increasingly observed in many diseases, but a deeper, mechanistic understanding of the cellular impact of altered iron metabolism is still lacking. In addition, deficits in neuronal energy metabolism due to reduced glucose import were described for Alzheimer’s disease (AD) and its comorbidities like obesity, depression, cardiovascular disease, and type 2 diabetes mellitus. The aim of this review is to present the molecular link between both observations. Insufficient cellular glucose uptake triggers increased ferritin expression, leading to depletion of the cellular free iron pool and stabilization of the hypoxia-induced factor (HIF) 1α. This transcription factor induces the expression of the glucose transporters (Glut) 1 and 3 and shifts the cellular metabolism towards glycolysis. If this first line of defense is not adequate for sufficient glucose supply, further reduction of the intracellular iron pool affects the enzymes of the mitochondrial electron transport chain and activates the AMP-activated kinase (AMPK). This enzyme triggers the translocation of Glut4 to the plasma membrane as well as the autophagic recycling of cell components in order to mobilize energy resources. Moreover, AMPK activates the autophagic process of ferritinophagy, which provides free iron urgently needed as a cofactor for the synthesis of heme- and iron–sulfur proteins. Excessive activation of this pathway ends in ferroptosis, a special iron-dependent form of cell death, while hampered AMPK activation steadily reduces the iron pools, leading to hypoferremia with iron sequestration in the spleen and liver. Long-lasting iron depletion affects erythropoiesis and results in anemia of chronic disease, a common condition in patients with AD and its comorbidities. Instead of iron supplementation, drugs, diet, or phytochemicals that improve energy supply and cellular glucose uptake should be administered to counteract hypoferremia and anemia of chronic disease. Full article
(This article belongs to the Special Issue 10th Anniversary of Biomedicines—Molecular Mechanisms and Treatments on Neurodegenerative Diseases)
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18 pages, 962 KiB  
Review
Gene-Based Therapeutics for Parkinson’s Disease
by Karim E. Shalaby and Omar M. A. El-Agnaf
Biomedicines 2022, 10(8), 1790; https://doi.org/10.3390/biomedicines10081790 - 26 Jul 2022
Cited by 3 | Viewed by 2340
Abstract
Parkinson’s disease (PD) is a complex multifactorial disorder that is not yet fully surmised, and it is only when such a disease is tackled on multiple levels simultaneously that we should expect to see fruitful results. Gene therapy is a modern medical practice [...] Read more.
Parkinson’s disease (PD) is a complex multifactorial disorder that is not yet fully surmised, and it is only when such a disease is tackled on multiple levels simultaneously that we should expect to see fruitful results. Gene therapy is a modern medical practice that theoretically and, so far, practically, has demonstrated its capability in joining the battle against PD and other complex disorders on most if not all fronts. This review discusses how gene therapy can efficiently replace current forms of therapy such as drugs, personalized medicine or invasive surgery. Furthermore, we discuss the importance of enhancing delivery techniques to increase the level of transduction and control of gene expression or tissue specificity. Importantly, the results of current trials establish the safety, efficacy and applicability of gene therapy for PD. Gene therapy’s variety of potential in interfering with PD’s pathology by improving basal ganglial circuitry, enhancing dopamine synthesis, delivering neuroprotection or preventing neurodegeneration may one day achieve symptomatic benefit, disease modification and eradication. Full article
(This article belongs to the Special Issue 10th Anniversary of Biomedicines—Molecular Mechanisms and Treatments on Neurodegenerative Diseases)
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26 pages, 1069 KiB  
Review
Disruption of the Ubiquitin-Proteasome System and Elevated Endoplasmic Reticulum Stress in Epilepsy
by Sarah Poliquin and Jing-Qiong Kang
Biomedicines 2022, 10(3), 647; https://doi.org/10.3390/biomedicines10030647 - 11 Mar 2022
Cited by 11 | Viewed by 3020
Abstract
The epilepsies are a broad group of conditions characterized by repeated seizures, and together are one of the most common neurological disorders. Additionally, epilepsy is comorbid with many neurological disorders, including lysosomal storage diseases, syndromic intellectual disability, and autism spectrum disorder. Despite the [...] Read more.
The epilepsies are a broad group of conditions characterized by repeated seizures, and together are one of the most common neurological disorders. Additionally, epilepsy is comorbid with many neurological disorders, including lysosomal storage diseases, syndromic intellectual disability, and autism spectrum disorder. Despite the prevalence, treatments are still unsatisfactory: approximately 30% of epileptic patients do not adequately respond to existing therapeutics, which primarily target ion channels. Therefore, new therapeutic approaches are needed. Disturbed proteostasis is an emerging mechanism in epilepsy, with profound effects on neuronal health and function. Proteostasis, the dynamic balance of protein synthesis and degradation, can be directly disrupted by epilepsy-associated mutations in various components of the ubiquitin-proteasome system (UPS), or impairments can be secondary to seizure activity or misfolded proteins. Endoplasmic reticulum (ER) stress can arise from failed proteostasis and result in neuronal death. In light of this, several treatment modalities that modify components of proteostasis have shown promise in the management of neurological disorders. These include chemical chaperones to assist proper folding of proteins, inhibitors of overly active protein degradation, and enhancers of endogenous proteolytic pathways, such as the UPS. This review summarizes recent work on the pathomechanisms of abnormal protein folding and degradation in epilepsy, as well as treatment developments targeting this area. Full article
(This article belongs to the Special Issue 10th Anniversary of Biomedicines—Molecular Mechanisms and Treatments on Neurodegenerative Diseases)
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