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21st Century Alzheimer’s Disease: Recent Advances and Future Challenges
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21st Century Alzheimer’s Disease: Recent Advances and Future Challenges

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 August 2023) | Viewed by 10934

Special Issue Editor

Dr. Vasileios Papaliagkas

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Guest Editor
Associate Professor of Physiology, Department of Biomedical Sciences, School of Health Sciences, International Hellenic University, 57400 Thessaloniki, Greece
Interests: Alzheimer’s disease; mild cognitive impairment; cerebrospinal fluid; beta amyloid; neurodegenerative diseases; neurodegeneration; cognition disorders; event-related potentials; evoked potentials
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Alzheimer’s disease (AD) is a neurodegenerative disease with a rising incidence among elderly people. It was first described in 1906 by a clinical psychiatrist and neuroanatomist named Alois Alzheimer. AD is the most common form of dementia and is characterized by progressive memory impairment. The neuropathological hallmarks of the disease are amyloid plaques comprising beta-amyloid and neurofibrillary tangles, which consist of the phosphorylated form of tau protein. It is a multifactorial disease with many genetic and molecular factors involved in its pathophysiology.

In this Special Issue, we welcome contributions in the form of original research, review articles and case reports on the study of diagnostic and prognostic biomarkers of AD (neurophysiological, genetic, neuroimaging) as well as articles examining novel methods and future prospects for AD diagnosis and treatment.

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

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • Alzheimer’s disease
  • mild cognitive impairment
  • neurophysiology
  • beta-amyloid
  • tau protein
  • EEG
  • transcranial magnetic stimulation

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Published Papers (2 papers)

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Research

18 pages, 1930 KiB  
Article
APOE Locus-Associated Mitochondrial Function and Its Implication in Alzheimer’s Disease and Aging
by Eun-Gyung Lee, Lesley Leong, Sunny Chen, Jessica Tulloch and Chang-En Yu
Int. J. Mol. Sci. 2023, 24(13), 10440; https://doi.org/10.3390/ijms241310440 - 21 Jun 2023
Cited by 7 | Viewed by 1864
Abstract
The Apolipoprotein E (APOE) locus has garnered significant clinical interest because of its association with Alzheimer’s disease (AD) and longevity. This genetic association appears across multiple genes in the APOE locus. Despite the apparent differences between AD and longevity, both conditions share [...] Read more.
The Apolipoprotein E (APOE) locus has garnered significant clinical interest because of its association with Alzheimer’s disease (AD) and longevity. This genetic association appears across multiple genes in the APOE locus. Despite the apparent differences between AD and longevity, both conditions share a commonality of aging-related changes in mitochondrial function. This commonality is likely due to accumulative biological effects partly exerted by the APOE locus. In this study, we investigated changes in mitochondrial structure/function-related markers using oxidative stress-induced human cellular models and postmortem brains (PMBs) from individuals with AD and normal controls. Our results reveal a range of expressional alterations, either upregulated or downregulated, in these genes in response to oxidative stress. In contrast, we consistently observed an upregulation of multiple APOE locus genes in all cellular models and AD PMBs. Additionally, the effects of AD status on mitochondrial DNA copy number (mtDNA CN) varied depending on APOE genotype. Our findings imply a potential coregulation of APOE locus genes possibly occurring within the same topologically associating domain (TAD) of the 3D chromosome conformation. The coordinated expression of APOE locus genes could impact mitochondrial function, contributing to the development of AD or longevity. Our study underscores the significant role of the APOE locus in modulating mitochondrial function and provides valuable insights into the underlying mechanisms of AD and aging, emphasizing the importance of this locus in clinical research. Full article
(This article belongs to the Special Issue 21st Century Alzheimer’s Disease: Recent Advances and Future Challenges)
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16 pages, 5291 KiB  
Article
The Cannabinoids, CBDA and THCA, Rescue Memory Deficits and Reduce Amyloid-Beta and Tau Pathology in an Alzheimer’s Disease-like Mouse Model
by Juyong Kim, Pilju Choi, Young-Tae Park, Taejung Kim, Jungyeob Ham and Jin-Chul Kim
Int. J. Mol. Sci. 2023, 24(7), 6827; https://doi.org/10.3390/ijms24076827 - 6 Apr 2023
Cited by 15 | Viewed by 8579
Abstract
Most studies related to hemp are focused on Cannabidiol (CBD) and Tetrahydrocannabinol (THC); however, up to 120 types of phytocannabinoids are present in hemp. Hemp leaves contain large amounts of Cannabidiolic acid (CBDA) and Tetrahydrocannabinolic acid (THCA), which are acidic variants of CBD [...] Read more.
Most studies related to hemp are focused on Cannabidiol (CBD) and Tetrahydrocannabinol (THC); however, up to 120 types of phytocannabinoids are present in hemp. Hemp leaves contain large amounts of Cannabidiolic acid (CBDA) and Tetrahydrocannabinolic acid (THCA), which are acidic variants of CBD and THC and account for the largest proportion of CBDA. In recent studies, CBDA exhibited anti-hyperalgesia and anti-inflammatory effects. THCA also showed anti-inflammatory and neuroprotective effects that may be beneficial for treating neurodegenerative diseases. CBDA and THCA can penetrate the blood–brain barrier (BBB) and affect the central nervous system. The purpose of this study was to determine whether CBDA and THCA ameliorate Alzheimer’s disease (AD)-like features in vitro and in vivo. The effect of CBDA and THCA was evaluated in the Aβ1–42-treated mouse model. We observed that Aβ1–42-treated mice had more hippocampal Aβ and p-tau levels, pathological markers of AD, and loss of cognitive function compared with PBS-treated mice. However, CBDA- and THCA-treated mice showed decreased hippocampal Aβ and p-tau and superior cognitive function compared with Aβ1–42-treated mice. In addition, CBDA and THCA lowered Aβ and p-tau levels, alleviated calcium dyshomeostasis, and exhibited neuroprotective effects in primary neurons. Our results suggest that CBDA and THCA have anti-AD effects and mitigate memory loss and resilience to increased hippocampal Ca2+, Aβ, and p-tau levels. Together, CBDA and THCA may be useful therapeutic agents for treating AD. Full article
(This article belongs to the Special Issue 21st Century Alzheimer’s Disease: Recent Advances and Future Challenges)
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