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 1213

Special Issue Editor


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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

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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 (1 paper)

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Research

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
Viewed by 902
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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