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Biology
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Animal Models of Neurodegenerative Diseases
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Animal Models of Neurodegenerative Diseases

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Neuroscience".

Deadline for manuscript submissions: 1 June 2025 | Viewed by 8271

Special Issue Editor

Dr. Xiangyu Guo

E-Mail Website
Guest Editor
Guangdong Key Laboratory of Non-Human Primate Research, Guangdong-Hongkong-Macau Institute of CNS Regeneration, Jinan University, Guangzhou 510632, China
Interests: neurodegenerative diseases; animal models; gene editing; molecular imaging; pathology; molecular genetics; animal behavior

Special Issue Information

Dear Colleagues,

Neurodegenerative diseases (NDs), such as Alzheimer's disease (AD), amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), and Huntington's disease (HD), are currently affecting more than 20 million people globally. As medicine advances and life spans extend, the number of ND cases is expected to surge quickly in the near future. To date, there is no effective therapy that can cure, halt, or even delay pathological progression, which has posed tremendous financial and emotional burdens to patients’ families.

One possible reason for this dilemma is the scarceness of animal models that can accurately mimic disease pathogenesis, or the inappropriate interpretation of the results from animal models. Animal models are essential tools for preclinical research; NDs are generally initiated via the interaction of various cell types as well as central nerve system dialogue with the peripheral system, underscoring research at the organism level. As gene edition technology advances and clinical genetics findings increase, more ND animal models have been generated in the past decades, therefore bringing us more insights into ND pathogenesis.

This Special Issue aims to collect the latest research concerning ND animal model creation, new pathogenesis mechanism findings from ND animals, and artificial intelligence-based integrative analyses of previous models.

Authors are invited to submit original research articles, as well as opinion and review papers.

We look forward to receiving your contributions.

Dr. Xiangyu Guo
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. Biology 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 2700 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

  • neurodegenerative diseases
  • Alzheimer's disease
  • amyotrophic lateral sclerosis
  • Parkinson's disease
  • Huntington's disease
  • neuroscience
  • animal models
  • pathogenesis

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Published Papers (5 papers)

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Research

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15 pages, 3528 KiB  
Article
Antiepileptic Effects of Acorus tatarinowii Schott in a Rat Model of Epilepsy: Regulation of Metabolic Axes and Gut Microbiota
by Liang Chen, Jiaxin Li, Wenhui Zhang and Jiepeng Wang
Biology 2025, 14(5), 488; https://doi.org/10.3390/biology14050488 (registering DOI) - 29 Apr 2025
Abstract
As a phytotherapeutic agent with historical applications in epilepsy management, Acorus tatarinowii Schott (ATS) remains pharmacologically enigmatic, particularly regarding its pathophysiological mechanisms. This knowledge gap significantly hinders the clinical application of ATS-based treatments. To explore the potential of ATS in combating epileptogenesis, we [...] Read more.
As a phytotherapeutic agent with historical applications in epilepsy management, Acorus tatarinowii Schott (ATS) remains pharmacologically enigmatic, particularly regarding its pathophysiological mechanisms. This knowledge gap significantly hinders the clinical application of ATS-based treatments. To explore the potential of ATS in combating epileptogenesis, we utilized a pentylenetetrazole (PTZ)-induced chronic epilepsy rat model. Brain metabolomic analysis was performed by ultra-performance liquid chromatography coupled with mass spectrometry (UPLC/MS). Principal component analysis (PCA) and orthogonal projections to latent structures-discriminant analysis (OPLS-DA) were performed for screening differential metabolites. Gut microbiota composition was analyzed through 16S rRNA gene sequencing and examined using Spearman correlation analysis. The results show that oral ATS (50 mg/kg) significantly improved the seizure latency and pathology of rats with epilepsy. Ascorbate and aldarate metabolism, glycerophospholipid metabolism, arachidonic acid metabolism, and intestinal flora were crucial for ATS’s ability to counteract epilepsy. The therapeutic effects of ATS against epilepsy were investigated with brain metabolomics and gut microbiota analysis, providing the basis for further comprehensive research. Full article
(This article belongs to the Special Issue Animal Models of Neurodegenerative Diseases)
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13 pages, 7150 KiB  
Article
Changes in the Cyto- and Fibroarchitectonics of the Cerebellar Cortex in Rats Subjected to Extreme Physical Activity
by Evgenii Balakin, Ksenia Yurku, Viacheslav Kuropatkin, Alexander Izotov, Valeriya Nakhod and Vasiliy Pustovoyt
Biology 2024, 13(10), 840; https://doi.org/10.3390/biology13100840 - 19 Oct 2024
Viewed by 1120
Abstract
Physical overexertion surpassing the functional capacity of the nervous system causes the hyperactivation of the neural structures of the cerebellum. In turn, it causes the depletion of intracellular resources and progressive structural changes in cerebellar cells and fibers. These degenerative changes may lead [...] Read more.
Physical overexertion surpassing the functional capacity of the nervous system causes the hyperactivation of the neural structures of the cerebellum. In turn, it causes the depletion of intracellular resources and progressive structural changes in cerebellar cells and fibers. These degenerative changes may lead to cerebellar dysfunction, including the worsening of coordination, balance, and motor functions. In order to maintain the health and functioning of the cerebellum and the nervous system in general, one needs to avoid physical overexertion and have enough time to recover. Three major types of Purkinje cells were identified in control group animals. After the forced swimming test, animals had significant morphological changes in pyriform cells, granule cells, internuncial neurons, and neuroglial cells. In particular, the extreme degeneration of granule cells was manifested via their fusion into conglomerates. These changes demonstrate that neurodegeneration in the cerebellum takes place in response to physical overexertion. Full article
(This article belongs to the Special Issue Animal Models of Neurodegenerative Diseases)
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19 pages, 8699 KiB  
Article
Exercise Promotes Hippocampal Neurogenesis in T2DM Mice via Irisin/TLR4/MyD88/NF-κB-Mediated Neuroinflammation Pathway
by Haocheng Xu, Xin Tian, Yuanxin Wang, Junjie Lin, Baishu Zhu, Chen Zhao, Bin Wang, Xin Zhang, Yu Sun, Nan Li, Xun Sun, Fanxi Zeng, Mingzhi Li, Xiquan Ya and Renqing Zhao
Biology 2024, 13(10), 809; https://doi.org/10.3390/biology13100809 - 10 Oct 2024
Viewed by 2161
Abstract
Neuroinflammation is a major feature of type 2 diabetic mellitus (T2DM), adversely affecting hippocampal neurogenesis. However, the precise mechanism is not fully understood, and therapeutic approaches are currently lacking. Therefore, we determined the effects of exercise on neuroinflammation and hippocampal neurogenesis in T2DM [...] Read more.
Neuroinflammation is a major feature of type 2 diabetic mellitus (T2DM), adversely affecting hippocampal neurogenesis. However, the precise mechanism is not fully understood, and therapeutic approaches are currently lacking. Therefore, we determined the effects of exercise on neuroinflammation and hippocampal neurogenesis in T2DM mice, with a specific focus on understanding the role of the irisin and related cascade pathways in modulating the beneficial effects of exercise in these processes. Ten-week exercise significantly decreased T2DM-induced inflammation levels and markedly promoted hippocampal neurogenesis and memory function. However, these positive effects were reversed by 10 weeks of treatment with cyclo RGDyk, an inhibitor of irisin receptor signaling. Additionally, exercise helped reduce the M1 phenotype polarization of hippocampal microglia in diabetic mice; this effect could be reversed with cyclo RGDyk treatment. Moreover, exercise markedly increased the levels of fibronectin type III domain-containing protein 5 (FNDC5)/irisin protein while decreasing the expression of Toll-like receptor 4 (TLR4), myeloid differential protein-88 (MyD88), and nuclear factor kappa-B (NF-κB) in the hippocampus of T2DM mice. However, blocking irisin receptor signaling counteracted the down-regulation of TLR4/MyD88/NF-κB in diabetic mice undergoing exercise intervention. Conclusively, exercise appears to be effective in reducing neuroinflammation and enhancing hippocampal neurogenesis and memory in diabetes mice. The positive effects are involved in the participation of the irisin/TLR4/MyD88/NF-κB signaling pathway, highlighting the potential of exercise in the management of diabetic-induced cognitive decline. Full article
(This article belongs to the Special Issue Animal Models of Neurodegenerative Diseases)
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17 pages, 1182 KiB  
Article
Neuroprotective Effect of Marrubium vulgare Extract in Scopolamine-Induced Cognitive Impairment in Rats: Behavioral and Biochemical Approaches
by Maria Lazarova, Miroslava Stefanova, Petko Denev, Teodora Taseva, Valya Vassileva and Krasimira Tasheva
Biology 2024, 13(6), 426; https://doi.org/10.3390/biology13060426 - 9 Jun 2024
Cited by 4 | Viewed by 2135
Abstract
The potential of Marrubium vulgare to alleviate scopolamine (Sco)-induced deficits in spatial working memory has drawn considerable scientific interest. This effect is partly attributed to its potent antioxidant and acetylcholinesterase inhibitory (AChEI) activities. This study examined the effects of M. vulgare extract, standardized [...] Read more.
The potential of Marrubium vulgare to alleviate scopolamine (Sco)-induced deficits in spatial working memory has drawn considerable scientific interest. This effect is partly attributed to its potent antioxidant and acetylcholinesterase inhibitory (AChEI) activities. This study examined the effects of M. vulgare extract, standardized to marrubiin content, on recognition memory in healthy and Sco-treated rats. Male Wistar rats (200–250 g) were divided into four groups. The extract was orally administered for 21 days and Sco (2 mg/kg) was intraperitoneally injected for 11 consecutive days. Memory performance was assessed using the novel object recognition test. Levels of acetylcholine (ACh), noradrenaline (NA), serotonin (Sero), and brain-derived neurotrophic factor (BDNF) and the phosphorylation of cAMP response element-binding protein (p-CREB) were evaluated in the cortex and hippocampus via ELISA. BDNF and CREB expression levels were assessed using RT-PCR. The results showed that M. vulgare significantly alleviated Sco-induced memory impairment, preserved cholinergic function in the hippocampus, increased NA levels in the brain, and restored pCREB expression in the cortex following Sco-induced reduction. In healthy rats, the extract upregulated BDNF, pCREB, and Bcl2 expression. Our findings indicate that the neuroprotective effects of M. vulgare may be linked to the modulation of cholinergic function, regulation of NA neurotransmission, and influence on key memory-related molecules. Full article
(This article belongs to the Special Issue Animal Models of Neurodegenerative Diseases)
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Review

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41 pages, 1012 KiB  
Review
Investigating the Interplay between Cardiovascular and Neurodegenerative Disease
by Jason Patrick Cousineau, Aimee Maria Dawe and Melanie Alpaugh
Biology 2024, 13(10), 764; https://doi.org/10.3390/biology13100764 - 26 Sep 2024
Cited by 2 | Viewed by 2210
Abstract
Neurological diseases, including neurodegenerative diseases (NDDs), are the primary cause of disability worldwide and the second leading cause of death. The chronic nature of these conditions and the lack of disease-modifying therapies highlight the urgent need for developing effective therapies. To accomplish this, [...] Read more.
Neurological diseases, including neurodegenerative diseases (NDDs), are the primary cause of disability worldwide and the second leading cause of death. The chronic nature of these conditions and the lack of disease-modifying therapies highlight the urgent need for developing effective therapies. To accomplish this, effective models of NDDs are required to increase our understanding of underlying pathophysiology and for evaluating treatment efficacy. Traditionally, models of NDDs have focused on the central nervous system (CNS). However, evidence points to a relationship between systemic factors and the development of NDDs. Cardiovascular disease and related risk factors have been shown to modify the cerebral vasculature and the risk of developing Alzheimer’s disease. These findings, combined with reports of changes to vascular density and blood–brain barrier integrity in other NDDs, such as Huntington’s disease and Parkinson’s disease, suggest that cardiovascular health may be predictive of brain function. To evaluate this, we explore evidence for disruptions to the circulatory system in murine models of NDDs, evidence of disruptions to the CNS in cardiovascular disease models and summarize models combining cardiovascular disruption with models of NDDs. In this study, we aim to increase our understanding of cardiovascular disease and neurodegeneration interactions across multiple disease states and evaluate the utility of combining model systems. Full article
(This article belongs to the Special Issue Animal Models of Neurodegenerative Diseases)
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