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Molecular Research on Neuroinflammation and Brain Aging

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

Deadline for manuscript submissions: 30 March 2025 | Viewed by 958

Special Issue Editor


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Guest Editor
Center for Occupational and Environmental Health, Department of Medicine, University of California, Irvine 100 Theory, Suite 100, Irvine, CA 92617-1830, USA
Interests: neurotoxicology; nutririon; aging; protein aggregates
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Aging is an ever-growing global issue as people now tend to live longer. One of the more tragic consequences of expanded longevity is the incidence of neurodegenerative disease present in people who are otherwise healthy. Managing the end-of-life care of those suffering from Alzheimer's disease is a rapidly growing problem that is both stressful and expensive. Specific maladies affecting the aging brain are based and dependent on a range of normal events associated with neurosenescence. One of the main processes characterizing even a healthy aging brain is the gradual malfunctioning of immune function, leading to a chronic state of inflammation that lacks a specific target and is, thus, unproductive. The harmfulness of such random activity in cerebral tissues, is further exacerbated in many neurodegenerative disorders.  A contributory factor underlying these events may be related to the brain’s inability to 'forget' a transient inflammatory stimulus, thus failing to fully restore immune activity to the resting state.  This Special Issue is devoted to furthering our mechanistic understanding of these progressive changes, thereby allowing for a rational approach to mitigating or delaying their undesirable consequences.

Prof. Dr. Stephen C. Bondy
Guest Editor

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Keywords

  • neurotoxicology
  • aging
  • Alzheimer's disease

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Published Papers (1 paper)

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Review

16 pages, 1045 KiB  
Review
The Critical Role of Autophagy and Phagocytosis in the Aging Brain
by Stephen C. Bondy and Meixia Wu
Int. J. Mol. Sci. 2025, 26(1), 57; https://doi.org/10.3390/ijms26010057 - 25 Dec 2024
Viewed by 711
Abstract
As the organism ages, there is a decline in effective energy supply, and this retards the ability to elaborate new proteins. The consequences of this are especially marked in the gradual decline in brain function. The senescence of cells and their constituent organelles [...] Read more.
As the organism ages, there is a decline in effective energy supply, and this retards the ability to elaborate new proteins. The consequences of this are especially marked in the gradual decline in brain function. The senescence of cells and their constituent organelles is ultimately the cause of aging of the entire nervous system. What is less immediately obvious is that brain aging is also accompanied by the failure of catabolic events that lead to the removal of non-functional cells and ineffective subcellular components. The removal of non-working cellular and subcellular elements within the brain is essential in order to allow the appearance of fresh cells and organelles with a full range of capacities. Thus, the maintenance of operative mechanisms for the dispersal of failed tissue components is important, and its diminished capacity with aging is a significant contributory factor to the onset and progression of age-related neurological disorder. This report discusses the mechanisms underlying autophagy and phagocytosis and how these can be adversely modulated as aging proceeds. The means by which the effective recycling of cellular components may be reinstated in the aged brain are considered. Full article
(This article belongs to the Special Issue Molecular Research on Neuroinflammation and Brain Aging)
Show Figures

Figure 1

Figure 1
<p>Autophagy and phagocytosis: breakdown of failed cells and cellular constituents resulting in beneficial metabolic changes and maintenance of cellular efficiency.</p>
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<p>Phagocytic and autophagic pathways that may experience excessive demand, leading to inflammation and potentially harmful neurodegenerative changes.</p>
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<p>Critical decision points distinguishing healthy brain aging from pathological age-related developments.</p>
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