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Pharmaceuticals
Special Issues
New Perspective in Alzheimer's Disease Treatment
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New Perspective in Alzheimer's Disease Treatment

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

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 5461

Special Issue Editors

Dr. Giulia Sita

E-Mail Website
Guest Editor
Department of Pharmacy and Biotechnology, University of Bologna, Bologna, Italy
Interests: neuroprotection; neurodegeneration; Alzheimer’s disease; oxidative stress; aging; neuroinflammation
Special Issues, Collections and Topics in MDPI journals
Dr. Fabiana Morroni

E-Mail Website
Guest Editor
Department of Pharmacy and Biotechnology, University of Bologna, Bologna, Italy
Interests: neurodegeneration; neuroprotection; neuropharmacology; neurotoxicology; neuroinflammation
Dr. Agnese Graziosi

E-Mail Website
Guest Editor
Department of Pharmacy and Biotechnology, University of Bologna, Bologna, Italy
Interests: neurodegeneration; neuroprotection; neuropharmacology; neurotoxicology; neuroinflammation

Special Issue Information

Dear Colleagues,

Alzheimer’s disease (AD) is the most common neurodegenerative disease that represents the principal cause of dementia worldwide. The social and economic burden behind this disease affects families, caregivers, and, obviously, patients. Numerous factors are involved in the onset and progression of AD, beyond the accumulation of β-amyloid (Aβ) protein and the formation of neurofibrillary tangles of tau protein, also neuroinflammation and the aging process play a fundamental role. Therefore, a multi-level approach is needed to fully capture the complex AD pathophysiology. Moreover, there is an urgent need to find reliable biomarkers to timely predict AD’s pathogenesis and to design new potential therapeutic strategies for the early stages of disease treatment able to counteract the evolution of the pathology. Thus, the identification of modifications that accumulate with aging in the AD brain is certainly needed to discover new successful therapeutic approaches. In this Special Issue, “New Perspective in Alzheimer's Disease Treatment”, we invite investigators to contribute original research articles and review articles regarding the novel therapeutic approaches to counteract AD progression.

Dr. Giulia Sita
Dr. Fabiana Morroni
Dr. Agnese Graziosi
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 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. 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

  • neurodegeneration
  • Alzheimer’s disease
  • drug discovery
  • neuroinflammation
  • therapeutics

Published Papers (2 papers)

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Research

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21 pages, 3138 KiB  
Article
Dapagliflozin Ameliorates Cognitive Impairment in Aluminum-Chloride-Induced Alzheimer’s Disease via Modulation of AMPK/mTOR, Oxidative Stress and Glucose Metabolism
by Waad A. Samman, Salma M. Selim, Hassan M. El Fayoumi, Norhan M. El-Sayed, Eman T. Mehanna and Reem M. Hazem
Pharmaceuticals 2023, 16(5), 753; https://doi.org/10.3390/ph16050753 - 16 May 2023
Cited by 7 | Viewed by 2453
Abstract
Alzheimer’s disease (AD) is a progressive neurological illness characterized by memory loss and cognitive deterioration. Dapagliflozin was suggested to attenuate the memory impairment associated with AD; however, its mechanisms were not fully elucidated. This study aims to examine the possible mechanisms of the [...] Read more.
Alzheimer’s disease (AD) is a progressive neurological illness characterized by memory loss and cognitive deterioration. Dapagliflozin was suggested to attenuate the memory impairment associated with AD; however, its mechanisms were not fully elucidated. This study aims to examine the possible mechanisms of the neuroprotective effects of dapagliflozin against aluminum chloride (AlCl3)-induced AD. Rats were distributed into four groups: group 1 received saline, group 2 received AlCl3 (70 mg/kg) daily for 9 weeks, and groups 3 and 4 were administered AlCl3 (70 mg/kg) daily for 5 weeks. Dapagliflozin (1 mg/kg) and dapagliflozin (5 mg/kg) were then given daily with AlCl3 for another 4 weeks. Two behavioral experiments were performed: the Morris Water Maze (MWM) and the Y-maze spontaneous alternation (Y-maze) task. Histopathological alterations in the brain, as well as changes in acetylcholinesterase (AChE) and amyloid β (Aβ) peptide activities and oxidative stress (OS) markers, were all evaluated. A western blot analysis was used for the detection of phosphorylated 5’ AMP-activated protein kinase (p-AMPK), phosphorylated mammalian target of Rapamycin (p-mTOR) and heme oxygenase-1 (HO-1). Tissue samples were collected for the isolation of glucose transporters (GLUTs) and glycolytic enzymes using PCR analysis, and brain glucose levels were also measured. The current data demonstrate that dapagliflozin represents a possible approach to combat AlCl3-induced AD in rats through inhibiting oxidative stress, enhancing glucose metabolism and activating AMPK signaling. Full article
(This article belongs to the Special Issue New Perspective in Alzheimer's Disease Treatment)
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Review

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17 pages, 11868 KiB  
Review
Protein Interactome of Amyloid-β as a Therapeutic Target
by Vladimir F. Lazarev, Elizaveta A. Dutysheva, Igor E. Kanunikov, Irina V. Guzhova and Boris A. Margulis
Pharmaceuticals 2023, 16(2), 312; https://doi.org/10.3390/ph16020312 - 16 Feb 2023
Cited by 4 | Viewed by 2621
Abstract
The amyloid concept of Alzheimer’s disease (AD) assumes the β-amyloid peptide (Aβ) as the main pathogenic factor, which injures neural and other brain cells, causing their malfunction and death. Although Aβ has been documented to exert its cytotoxic effect in a solitary manner, [...] Read more.
The amyloid concept of Alzheimer’s disease (AD) assumes the β-amyloid peptide (Aβ) as the main pathogenic factor, which injures neural and other brain cells, causing their malfunction and death. Although Aβ has been documented to exert its cytotoxic effect in a solitary manner, there is much evidence to claim that its toxicity can be modulated by other proteins. The list of such Aβ co-factors or interactors includes tau, APOE, transthyretin, and others. These molecules interact with the peptide and affect the ability of Aβ to form oligomers or aggregates, modulating its toxicity. Thus, the list of potential substances able to reduce the harmful effects of the peptide should include ones that can prevent the pathogenic interactions by specifically binding Aβ and/or its partners. In the present review, we discuss the data on Aβ-based complexes in AD pathogenesis and on the compounds directly targeting Aβ or the destructors of its complexes with other polypeptides. Full article
(This article belongs to the Special Issue New Perspective in Alzheimer's Disease Treatment)
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