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Editorial Board Members’ Collection Series: “Molecular Research in Dementia”

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Neurobiology".

Deadline for manuscript submissions: closed (31 July 2024) | Viewed by 1215

Special Issue Editors


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Guest Editor
Laboratory of Neuronal Networks Morphology and System Biology, Department of Mental and Physical Health and Preventive Medicine, University of Campania ‘‘Luigi Vanvitelli”, 80138 Naples, Italy
Interests: neuroinflammation; astrocytes; synaptic plasticity; nerve growth factor; vagus nerve stimulation
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Guest Editor
Department of Neurology, Sant’Elia Hospital, ASP Caltanissetta, Via Luigi Russo, 6-93100 Caltanissetta, Italy
Interests: clinical neurophysiology; clinical neurology; neurophysiology; brain diseases; TMS; brain stimulation; neurological diseases; neuroplasticity; neurostimulation; neuromodulation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue aims to attract the interest of researchers who study the molecular mechanism of dementia. Understanding the molecular mechanisms of dementia involves exploring various aspects of cellular and molecular biology. Below is a list of potential topics that focus on molecule-level studies related to impaired memory, signaling pathways, and the impact of neurotransmitters and neuromodulators in different brain structures:

  1. Amyloid Beta and Tau Proteins: Investigate the role of amyloid beta and tau proteins in the formation of plaque and neurofibrillary tangles, respectively, in Alzheimer's disease.

Explore the molecular mechanisms underlying the aggregation of these proteins and their impact on synaptic function and memory.

  1. Neuroinflammation: Examine the involvement of microglia and astrocytes in neuroinflammation associated with dementia. Explore the molecular signals that trigger and sustain chronic inflammation in the brain, and its impact on cognitive function.
  2. Synaptic Dysfunction: Investigate the molecular mechanisms underlying synaptic dysfunction in dementia, including alterations in neurotransmitter release, receptor expression, and synaptic plasticity. Explore the role of key synaptic proteins and their interactions in maintaining normal synaptic function.
  3. Cellular Signaling Pathways: Explore specific cellular signaling pathways implicated in dementia, such as the Wnt/β-catenin pathway, Notch signaling, and MAPK/ERK pathway.

Investigate how dysregulation of these pathways contributes to cognitive decline and memory impairment.

  1. Neurotransmitter Imbalance: Examine the impact of neurotransmitter imbalances, such as acetylcholine deficiency in Alzheimer's disease, on cognitive function. Explore the molecular mechanisms underlying the dysregulation of neurotransmitter systems and potential therapeutic targets.
  2. Neuromodulators and Neurotransmitter Receptors: Investigate the role of neuromodulators, such as dopamine, serotonin, and norepinephrine, in modulating cognitive processes and memory formation. Explore changes in neurotransmitter receptor expression and function in different brain regions associated with dementia.
  3. Epigenetic Modifications: Explore how epigenetic modifications, such as DNA methylation and histone acetylation, influence gene expression in dementia. Investigate the impact of environmental factors on epigenetic regulation and their contribution to cognitive decline.
  4. Mitochondrial Dysfunction: Examine the molecular mechanisms underlying mitochondrial dysfunction in dementia, including oxidative stress, impaired energy production, and mitochondrial DNA damage. Explore the interplay between mitochondrial function and neuronal health.
  5. Neurovascular Unit Dysfunction: Investigate the molecular mechanisms linking vascular dysfunction and impaired blood–brain barrier integrity to dementia. Explore how compromised neurovascular unit function contributes to neurodegeneration and cognitive decline.
  6. Neurogenesis and Neural Stem Cells: Explore the role of neurogenesis and neural stem cells in dementia and cognitive decline. Investigate the molecular mechanisms influencing neurogenesis, neuronal differentiation, and integration into existing neural circuits.

It is essential to consider the latest research findings and advancements in the field of neuroscience. Interdisciplinary approaches that integrate genetics, biochemistry, neurophysiology, and imaging techniques can provide a comprehensive understanding of the molecular mechanisms underlying dementia.

Dr. Jana Tchekalarova
Prof. Dr. Michele Papa
Dr. Mariagiovanna Cantone
Guest Editors

Manuscript Submission Information

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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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

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Keywords

  • dementia
  • amyloid beta
  • tau proteins
  • neuroinflammation
  • synaptic dysfunction
  • mitochondrial dysfunction

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Published Papers (1 paper)

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20 pages, 3248 KiB  
Article
Tailored Melatonin- and Donepezil-Based Hybrids Targeting Pathognomonic Changes in Alzheimer’s Disease: An In Vitro and In Vivo Investigation
by Rositsa Mihaylova, Violina T. Angelova, Jana Tchekalarova, Dimitrinka Atanasova, Petja Ivanova and Rumyana Simeonova
Int. J. Mol. Sci. 2024, 25(11), 5969; https://doi.org/10.3390/ijms25115969 - 29 May 2024
Viewed by 944
Abstract
A plethora of pathophysiological events have been shown to play a synergistic role in neurodegeneration, revealing multiple potential targets for the pharmacological modulation of Alzheimer’s disease (AD). In continuation to our previous work on new indole- and/or donepezil-based hybrids as neuroprotective agents, the [...] Read more.
A plethora of pathophysiological events have been shown to play a synergistic role in neurodegeneration, revealing multiple potential targets for the pharmacological modulation of Alzheimer’s disease (AD). In continuation to our previous work on new indole- and/or donepezil-based hybrids as neuroprotective agents, the present study reports on the beneficial effects of lead compounds of the series on key pathognomonic features of AD in both cellular and in vivo models. An enzyme-linked immunosorbent assay (ELISA) was used to evaluate the anti-fibrillogenic properties of 15 selected derivatives and identify quantitative changes in the formation of neurotoxic β-amyloid (Aβ42) species in human neuronal cells in response to treatment. Among the most promising compounds were 3a and 3c, which have recently shown excellent antioxidant and anticholinesterase activities, and, therefore, have been subjected to further in vivo investigation in mice. An acute toxicity study was performed after intraperitoneal (i.p.) administration of both compounds, and 1/10 of the LD50 (35 mg/kg) was selected for subacute treatment (14 days) with scopolamine in mice. Donepezil (DNPZ) and/or galantamine (GAL) were used as reference drugs, aiming to establish any pharmacological superiority of the multifaceted approach in battling hallmark features of neurodegeneration. Our promising results give first insights into emerging disease-modifying strategies to combine multiple synergistic activities in a single molecule. Full article
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