Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
4.8
2.7
Journals
Brain Sciences
Special Issues
Cellular and Molecular Mechanisms in Brain Aging
share announcement

Cellular and Molecular Mechanisms in Brain Aging

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Molecular and Cellular Neuroscience".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 4558

Special Issue Editors

Dr. Giuseppe Lupo

E-Mail Website
Guest Editor
Department of Biology and Biotechnology "C. Darwin", Sapienza University of Rome, 00185 Rome, Italy
Interests: neural development; neural stem cells; neurogenesis; aging; gene regulation; morphogens; homeobox genes
Special Issues, Collections and Topics in MDPI journals
Dr. Maria Elena Miranda Banos

E-Mail Website
Guest Editor
Department of Biology and Biotechnology "C. Darwin", Sapienza University of Rome, 00185 Rome, Italy
Interests: neurodegeneration; neuronal cell death and stress; endoplasmic reticulum stress; protein aggregation; misfolded protein diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Aging is associated with cognitive decline and with increased susceptibility to neurodegenerative diseases, such as Alzheimer’s and Parkinson’s diseases, among others. The increasing life expectancy of the human population may result in large numbers of cognitively impaired elderly subjects, with a heavy burden on healthcare systems and huge social and financial challenges. The development of therapeutic approaches to mitigate the effects of aging on brain health and cognitive function requires a comprehensive knowledge of the age-related alterations to brain neuronal networks and the underlying mechanisms, which is still lacking. Furthermore, age-associated neuropathological conditions may involve an enhancement of the mechanisms driving physiological brain aging, a dysregulation of the protective mechanisms active in the aging brain, or both. Therefore, it is crucial to compare the alterations, and the mechanisms, implicated in physiological and pathological brain aging, and to identify common and diverging traits. This Special Issue is focused on the cellular and molecular alterations taking place during physiological and/or pathological brain aging, and on the elucidation of the mechanisms driving them. Submissions of both original research articles and review articles providing a critical discussion of recent progress in the field are welcome. Original research manuscripts providing mechanistic insights based on functional data are preferred, but descriptive studies will also be considered, as long as they do not duplicate previously published work.

Dr. Giuseppe Lupo
Dr. Maria Elena Miranda Banos
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. Brain Sciences 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 2200 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

  • neuronal death
  • neuronal dysfunction
  • neuroinflammation
  • astrocytes
  • microglia
  • brain vasculature
  • gene expression
  • protein folding and trafficking
  • cell signaling

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

33 pages, 5604 KiB  
Article
Metallothionein I/II Expression and Metal Ion Levels in Correlation with Amyloid Beta Deposits in the Aged Feline Brain
by Emmanouela P. Apostolopoulou, Nikolaos Raikos, Ioannis Vlemmas, Efstratios Michaelidis and Georgia D. Brellou
Brain Sci. 2023, 13(7), 1115; https://doi.org/10.3390/brainsci13071115 - 22 Jul 2023
Viewed by 2076
Abstract
Brain aging has been correlated with high metallothionein I-II (MT-I/II) expression, iron and zinc dyshomeostasis, and Aβ deposition in humans and experimental animals. In the present study, iron and zinc accumulation, the expression of MT-I/II and Aβ42, and their potential association with aging [...] Read more.
Brain aging has been correlated with high metallothionein I-II (MT-I/II) expression, iron and zinc dyshomeostasis, and Aβ deposition in humans and experimental animals. In the present study, iron and zinc accumulation, the expression of MT-I/II and Aβ42, and their potential association with aging in the feline brain were assessed. Tissue sections from the temporal and frontal grey (GM) and white (WM) matter, hippocampus, thalamus, striatum, cerebellum, and dentate nucleus were examined histochemically for the presence of age-related histopathological lesions and iron deposits and distribution. We found, using a modified Perl’s/DAB method, two types of iron plaques that showed age-dependent accumulation in the temporal GM and WM and the thalamus, along with the age-dependent increment in cerebellar-myelin-associated iron. We also demonstrated an age-dependent increase in MT-I/II immunoreactivity in the feline brain. In cats over 7 years old, Aβ immunoreactivity was detected in vessel walls and neuronal somata; extracellular Aβ deposits were also evident. Interestingly, Aβ-positive astrocytes were also observed in certain cases. ICP-MS analysis of brain content regarding iron and zinc concentrations showed no statistically significant association with age, but a mild increase in iron with age was noticed, while zinc levels were found to be higher in the Mature and Senior groups. Our findings reinforce the suggestion that cats could serve as a dependable natural animal model for brain aging and neurodegeneration; thus, they should be further investigated on the basis of metal ion concentration changes and their effects on aging. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Brain Aging)
►▼ Show Figures

Figure 1

16 pages, 2512 KiB  
Article
Rapamycin Affects the Hippocampal SNARE Complex to Alleviate Cognitive Dysfunction Induced by Surgery in Aged Rats
by Ning Kang, Xiaoguang Han, Zhengqian Li, Taotao Liu, Xinning Mi, Yue Li, Xiangyang Guo, Dengyang Han and Ning Yang
Brain Sci. 2023, 13(4), 598; https://doi.org/10.3390/brainsci13040598 - 31 Mar 2023
Cited by 2 | Viewed by 1845
Abstract
Delayed neurocognitive recovery (dNCR) is a common complication that occurs post-surgery, especially in elderly individuals. The soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex plays an essential role in various membrane fusion events, such as synaptic vesicle exocytosis and autophagosome–lysosome fusion. Although SNARE [...] Read more.
Delayed neurocognitive recovery (dNCR) is a common complication that occurs post-surgery, especially in elderly individuals. The soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE) complex plays an essential role in various membrane fusion events, such as synaptic vesicle exocytosis and autophagosome–lysosome fusion. Although SNARE complex dysfunction has been observed in several neurodegenerative disorders, the causal link between SNARE-mediated membrane fusion and dNCR remains unclear. We previously demonstrated that surgical stimuli caused cognitive impairment in aged rats by inducing α-synuclein accumulation, inhibiting autophagy, and disrupting neurotransmitter release in hippocampal synaptosomes. Here, we evaluated the effects of propofol anesthesia plus surgery on learning and memory and investigated levels of SNARE proteins and chaperones in hippocampal synaptosomes. Aged rats that received propofol anesthesia and surgery exhibited learning and memory impairments in a Morris water maze test and decreased levels of synaptosome-associated protein 25, synaptobrevin/vesicle-associated membrane protein 2, and syntaxin 1. Levels of SNARE chaperones, including mammalian uncoordinated-18, complexins 1 and 2, cysteine string protein-α, and N-ethylmaleimide-sensitive factor, were all significantly decreased following anesthesia with surgical stress. However, the synaptic vesicle marker synaptophysin was unaffected. The autophagy-enhancer rapamycin attenuated structural and functional disturbances of the SNARE complex and ameliorated disrupted neurotransmitter release. Our results indicate that perturbations of SNARE proteins in hippocampal synaptosomes may underlie the occurrence of dNCR. Moreover, the protective effect of rapamycin may partially occur through recovery of SNARE structural and functional abnormalities. Our findings provide insight into the molecular mechanisms underlying dNCR. Full article
(This article belongs to the Special Issue Cellular and Molecular Mechanisms in Brain Aging)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop