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Pharmaceuticals
Special Issues
Cholinergic Modulation, Anticholinergic Burden, and Neuroprotection: Mechanisms to Therapeutics
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Cholinergic Modulation, Anticholinergic Burden, and Neuroprotection: Mechanisms to Therapeutics

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: 25 March 2026 | Viewed by 2596

Special Issue Editors

Dr. Ion Brinza

E-Mail Website
Guest Editor
Faculty of Sciences, “Lucian Blaga” University of Sibiu, 7–9 Ion Ratiu Street, 550024 Sibiu, Romania
Interests: neuropharmacology and neuromodulation; oxidative stress and neurotransmitter dynamics; cognitive impairment and neurodegenerative diseases; bioactive compounds: flavonoids, polyphenols, and nutraceuticals; molecular docking and drug discovery; pharmacokinetics and drug delivery systems; laboratory animal behavior analysis using specialized software; environmental toxicology and ecotoxicological impact; zebrafish and other animal models in biomedical research; advanced laboratory techniques: western blot, PCR, HPLC, GC-MS, LC-MS/MS, antioxidant activity evaluation; AI-powered tools for data analysis, behavioral tracking, and drug discovery; nutrition and the role of bioactive compounds in metabolic and cognitive health
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Lucian Hritcu

E-Mail Website
Guest Editor
Faculty of Biology, Alexandru Ioan Cuza University of Iasi, Bd. Carol I, No. 11, 700506 Iasi, Romania
Interests: neurobiology; molecular biology; neuropharmacology; behavioral neuropsychopharmacology; phytomedicine and ethnopharmacology; neurodegenerative diseases (Parkinson, Alzheimer); brain aging
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cholinergic dysfunction remains a central driver of cognitive impairment across conditions ranging from Alzheimer’s disease and Parkinson’s disease dementia to postoperative delirium and chemotherapy-related cognitive change. Building on our initial focus on scopolamine—both as a therapeutic agent and a probe of cholinergic systems—this Special Issue broadens its scope to encompass the full cholinergic axis: molecular mechanisms, anticholinergic burden, compensatory neurotransmitter crosstalk, and multimodal interventions. We welcome preclinical and clinical contributions that clarify how anticholinergic agents (including scopolamine and related tropanes) influence synaptic plasticity, redox homeostasis, neuroinflammation, and network dynamics, as well as studies that de-risk these liabilities via targeted delivery, PK/PD optimization, and adjunctive neuroprotective strategies. Submissions leveraging bioactive compounds (flavonoids, polyphenols, nutraceuticals), systems pharmacology, computational modeling, and AI-assisted analytics are encouraged. We also invite work on biomarkers (imaging, fluid, and digital behavior), anticholinergic burden quantification, and mitigation in vulnerable populations. By integrating mechanistic insights with translational endpoints, this collection aims to chart practical paths from bench concepts to clinically meaningful cognitive outcomes.

Suggested topics (concise):

  • Scopolamine and related anticholinergics: therapeutic uses, liabilities, and mitigation;
  • Anticholinergic burden indices and outcomes (elderly, peri-operative, oncology, psychiatry);
  • Cholinergic–glutamatergic/dopaminergic/adrenergic crosstalk in cognition;
  • Oxidative stress, mitochondrial signaling, and neuroinflammation under anticholinergic challenge;
  • Targeted delivery, prodrugs, micro/nano-carriers; PK/PD and BBB transport;
  • Bioactive compounds and combination strategies that offset anticholinergic effects;
  • Biomarkers: EEG/MEG, fMRI, PET ligands, CSF/plasma markers, digital phenotyping;
  • Computational pharmacology, docking, network models, and AI-assisted behavioral tracking;
  • Zebrafish and rodent models; human challenge paradigms and early-phase trials;
  • Safety, deprescribing frameworks, and guidelines to reduce anticholinergic load.

Dr. Ion Brinza
Prof. Dr. Lucian Hritcu
Guest Editors

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 250 words) can be sent to the Editorial Office for assessment.

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. Pharmaceuticals 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 2900 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

  • scopolamine
  • anticholinergic burden
  • cholinergic modulation
  • cognitive impairment
  • neuroinflammation
  • oxidative stress
  • BBB/drug delivery
  • PK/PD
  • biomarkers
  • network pharmacology
  • flavonoids/polyphenols
  • zebrafish models
  • translational neuroscience
  • deprescribing

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Published Papers (2 papers)

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Research

19 pages, 5932 KB  
Article
Rubus occidentalis Ethanol Extract Attenuates Neuroinflammation and Cognitive Impairment in Lipopolysaccharide-Stimulated Microglia and Scopolamine-Induced Amnesic Mice
by Ga-Won Kim, Yon-Suk Kim, Tohmina Afroze Bondhon, Rengasamy Balakrishnan, Jun-Hyuk Han, Ji-Wung Kwon, Woo-Jung Kim and Dong-Kug Choi
Pharmaceuticals 2025, 18(10), 1557; https://doi.org/10.3390/ph18101557 - 16 Oct 2025
Viewed by 665
Abstract
Background/Objectives: Neuroinflammatory mechanisms, primarily mediated by activated microglia, play a key role in the progression of conditions such as mild cognitive impairment associated with Alzheimer’s disease. Rubus occidentalis (R. occidentalis), a black-fruited raspberry native to North America, is reported to possess [...] Read more.
Background/Objectives: Neuroinflammatory mechanisms, primarily mediated by activated microglia, play a key role in the progression of conditions such as mild cognitive impairment associated with Alzheimer’s disease. Rubus occidentalis (R. occidentalis), a black-fruited raspberry native to North America, is reported to possess antimicrobial, antidiabetic, and anticancer properties. This study investigated the neuroprotective and anti-neuroinflammatory effects of a 100% ethanol extract from premature R. occidentalis fruits (ROE) in lipopolysaccharide (LPS)-stimulated BV-2 microglial cells and a scopolamine-induced amnesic mouse model. Methods: C57BL/6N mice were orally administered ROE (100 or 200 mg/kg/b.w.) and donepezil (DNZ, 5 mg/kg) for 9 days and intraperitoneally injected with scopolamine (2 mg/kg/b.w.) for two days. Spatial learning and cognitive function were assessed using the Y-maze and Morris water maze tests. Protein and mRNA levels were examined both in vitro and in vivo through Western blotting and RT-PCR analysis. Results: In vitro, ROE improved cell viability and reduced nitric oxide overproduction in LPS-stimulated BV-2 cells, attenuated LPS-induced phosphorylation and degradation of IκB-α (thereby limiting NF-κB p65 nuclear translocation), and suppressed phosphorylation of MAPK signaling components. In vivo, ROE administration enhanced spatial learning and memory in scopolamine-treated C57BL/6N mice, increased hippocampal levels of brain-derived neurotrophic factor (BDNF) and phosphorylated CREB, and reduced the expression of iNOS and COX-2. Conclusions: Collectively, these results suggest that ROE possesses neuroprotective properties mediated by inhibition of NF-κB and MAPK signaling, promotion of CREB/BDNF pathways, and amelioration of neuroinflammation and cognitive deficits. Thus, ROE may represent a promising therapeutic candidate for neuroinflammatory disorders. Full article
(This article belongs to the Special Issue Cholinergic Modulation, Anticholinergic Burden, and Neuroprotection: Mechanisms to Therapeutics)
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26 pages, 6937 KB  
Article
Solanum macrocarpon L. Ethanolic Leaf Extract Exhibits Neuroprotective and Anxiolytic Effects in Scopolamine-Induced Amnesic Zebrafish Model
by Ion Brinza, Corina Guliev, Ibukun Oluwabukola Oresanya, Hasya Nazli Gok, Ilkay Erdogan Orhan and Lucian Hritcu
Pharmaceuticals 2025, 18(5), 706; https://doi.org/10.3390/ph18050706 - 9 May 2025
Cited by 4 | Viewed by 1222
Abstract
Background/Objectives: Solanum macrocarpon L. has been studied for its neuroprotective potential and memory-enhancing properties. Research suggests that bioactive compounds, including flavonoids, alkaloids, and phenolics, contribute to its cognitive benefits. These compounds may help protect against oxidative stress, neuroinflammation, and cholinergic dysfunction factors [...] Read more.
Background/Objectives: Solanum macrocarpon L. has been studied for its neuroprotective potential and memory-enhancing properties. Research suggests that bioactive compounds, including flavonoids, alkaloids, and phenolics, contribute to its cognitive benefits. These compounds may help protect against oxidative stress, neuroinflammation, and cholinergic dysfunction factors in memory impairment. This study was undertaken to investigate the effects of S. macrocarpon ethanolic leaf extract (SMEE) on the memory, anxiety-like behavior, and brain antioxidant status of scopolamine (SCOP, 100 μM)-induced amnesic zebrafish (Danio rerio) and thus to understand its possible mechanism of action. Methods: Adult zebrafish (n = 100) were divided into two cohorts (±SCOP) of five experimental groups: (I) control; (II) galantamine (GAL, 1 mg/L), serving as a positive control for both behavioral and biochemical assessments; (III–V) three groups treated with SMEE (1, 3, and 6 mg/L); (VI) scopolamine (SCOP, 100 μM); (VII) SCOP (100 μM) combined with GAL (1 mg/L); and (VIII–X) three groups treated with SCOP (100 μM) plus SMEE (1, 3, and 6 mg/L). The treatment lasted 23 days and amnesia was induced by a single dose of SCOP (100 μM) before testing. Results: The phenolic characterization from the samples was performed by using HPLC-PDA chromatography. Following HPLC analysis, an in silico pharmacokinetic evaluation was conducted using the ADMET model to investigate the pharmacological and toxicological profiles of the identified compounds. Spatial memory was evaluated through the Y-maze and novel object recognition (NOR) tests, while anxiety-like behavior was assessed using the novel tank diving test (NTT), novel approach test (NAT), and light–dark test (LDT). The zebrafish were euthanized, and homogenates of isolated brain samples were assayed for acetylcholinesterase (AChE) activity and brain antioxidant markers. The HPLC analysis revealed that the main major compounds in the extract were chlorogenic acid and rutin, both recognized for their significant antioxidant properties. Conclusions: SMEE enhanced memory by inhibiting AChE, alleviated SCOP-induced anxiety-like behavior, and significantly decreased oxidative stress markers. These findings support the potential role of SMEE in counteracting SCOP-induced cognitive and behavioral dysfunctions, related to dementia conditions. Full article
(This article belongs to the Special Issue Cholinergic Modulation, Anticholinergic Burden, and Neuroprotection: Mechanisms to Therapeutics)
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