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Biology
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New Concepts in Brain Aging, Alzheimer's Disease and Related Dementias
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New Concepts in Brain Aging, Alzheimer's Disease and Related Dementias

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Neuroscience".

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 5302

Special Issue Editor

Dr. Rupal Mehta

E-Mail Website
Guest Editor
Department of Pathology, Rush University Alzheimer’s Disease Center, Chicago, IL 60612, USA
Interests: advanced histology; aging; Alzheimer's disease; amyloid, aneurysm; autopsy; cerebrovascular diseases; dementia; histology; immunohistochemistry; proteinopathy; signaling; subarachnoid hemorrhage; stroke; vascular diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Alzheimer's disease and Alzheimer's-disease-related dementias (AD/ADRDs) are common diseases, and their incidence is rising in our aging populations. There are currently no known treatments to halt the progression of AD/ADRDs. However, knowledge on this group of diseases is increasing at a rapid pace. With new insights in neuroanatomy, neurophysiology, and age-associated changes in the brain, it is crucial to explore novel neuroinflammatory and other mechanism(s) responsible for neurodegeneration. This Special Issue focuses on the current state of the art and will highlight the current understanding of brain structure, roles and/or effects of neuroinflammation, and their associations with dementia progression. While therapeutic approaches remain limited, researchers are invited to share new articles, commentaries, cases, and/or reviews dealing with structural, molecular, genetic, and/or neuroimmunological changes that are involved in brain degeneration and/or that elucidate epidemiological links between inflammation, diet, stress, and dementia.

Potential topics include:

  • Basic research into molecular mechanisms of neuronal cell death.
  • Basic research into molecular mechanisms of neuronal stress signaling.
  • Basic research into cell death pathways involving other brain cells.
  • New preventative and/or management strategies for cognitive decline.
  • Evidence of lifestyle and/or dietary factors relevant to brain health and/or aging.
  • Identification of novel tissue markers and/or inflammatory mechanisms responsible for age-associated structural brain change.
  • Novel pattern(s) and/or type(s) of intracerebral protein aggregate deposition.

We look forward to receiving your contributions to this Special Issue, which will compile new developments in an exciting and fast-moving field.

Dr. Rupal Mehta
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. Biology 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 2700 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

  • Alzheimer's disease
  • amyloid
  • brain aging
  • cerebrovascular disease
  • dementia
  • diet
  • mixed pathologies
  • neuroprotection
  • proteinopathy
  • traumatic brain injury

Published Papers (3 papers)

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Research

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14 pages, 1303 KiB  
Article
Alzheimer’s Disease and Age-Related Changes in the Cu Isotopic Composition of Blood Plasma and Brain Tissues of the APPNL-G-F Murine Model Revealed by Multi-Collector ICP-Mass Spectrometry
by Kasper Hobin, Marta Costas-Rodríguez, Elien Van Wonterghem, Roosmarijn E. Vandenbroucke and Frank Vanhaecke
Biology 2023, 12(6), 857; https://doi.org/10.3390/biology12060857 - 14 Jun 2023
Viewed by 1251
Abstract
Alzheimer’s’ disease (AD) is characterized by the formation of β-amyloid (Aβ) plaques and neurofibrillary tangles of tau protein in the brain. Aβ plaques are formed by the cleavage of the β-amyloid precursor protein (APP). In addition to protein aggregations, the metabolism of the [...] Read more.
Alzheimer’s’ disease (AD) is characterized by the formation of β-amyloid (Aβ) plaques and neurofibrillary tangles of tau protein in the brain. Aβ plaques are formed by the cleavage of the β-amyloid precursor protein (APP). In addition to protein aggregations, the metabolism of the essential mineral element Cu is also altered during the pathogenesis of AD. The concentration and the natural isotopic composition of Cu were investigated in blood plasma and multiple brain regions (brain stem, cerebellum, cortex, and hippocampus) of young (3–4 weeks) and aged (27–30 weeks) APPNL-G-F knock-in mice and wild-type controls to assess potential alterations associated with ageing and AD. Tandem inductively coupled plasma-mass spectrometry (ICP-MS/MS) was used for elemental analysis and multi-collector inductively coupled plasma-mass spectrometry (MC-ICP-MS) for high-precision isotopic analysis. The blood plasma Cu concentration was significantly altered in response to both age- and AD-related effects, whereas the blood plasma Cu isotope ratio was only affected by the development of AD. Changes in the Cu isotopic signature of the cerebellum were significantly correlated with the changes observed in blood plasma. The brain stem showed a significant increase in Cu concentration for both young and aged AD transgenic mice compared with healthy controls, whereas the Cu isotopic signature became lighter as a result of age-related changes. In this work, ICP-MS/MS and MC-ICP-MS provided relevant and complementary information on the potential role of Cu in ageing and AD. Full article
(This article belongs to the Special Issue New Concepts in Brain Aging, Alzheimer's Disease and Related Dementias)
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Review

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23 pages, 1482 KiB  
Review
Role of NFE2L1 in the Regulation of Proteostasis: Implications for Aging and Neurodegenerative Diseases
by Aswathy Chandran, Haley Jane Oliver and Jean-Christophe Rochet
Biology 2023, 12(9), 1169; https://doi.org/10.3390/biology12091169 - 25 Aug 2023
Viewed by 1616
Abstract
A hallmark of aging and neurodegenerative diseases is a disruption of proteome homeostasis (“proteostasis”) that is caused to a considerable extent by a decrease in the efficiency of protein degradation systems. The ubiquitin proteasome system (UPS) is the major cellular pathway involved in [...] Read more.
A hallmark of aging and neurodegenerative diseases is a disruption of proteome homeostasis (“proteostasis”) that is caused to a considerable extent by a decrease in the efficiency of protein degradation systems. The ubiquitin proteasome system (UPS) is the major cellular pathway involved in the clearance of small, short-lived proteins, including amyloidogenic proteins that form aggregates in neurodegenerative diseases. Age-dependent decreases in proteasome subunit expression coupled with the inhibition of proteasome function by aggregated UPS substrates result in a feedforward loop that accelerates disease progression. Nuclear factor erythroid 2- like 1 (NFE2L1) is a transcription factor primarily responsible for the proteasome inhibitor-induced “bounce-back effect” regulating the expression of proteasome subunits. NFE2L1 is localized to the endoplasmic reticulum (ER), where it is rapidly degraded under basal conditions by the ER-associated degradation (ERAD) pathway. Under conditions leading to proteasome impairment, NFE2L1 is cleaved and transported to the nucleus, where it binds to antioxidant response elements (AREs) in the promoter region of proteasome subunit genes, thereby stimulating their transcription. In this review, we summarize the role of UPS impairment in aging and neurodegenerative disease etiology and consider the potential benefit of enhancing NFE2L1 function as a strategy to upregulate proteasome function and alleviate pathology in neurodegenerative diseases. Full article
(This article belongs to the Special Issue New Concepts in Brain Aging, Alzheimer's Disease and Related Dementias)
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Other

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16 pages, 331 KiB  
Systematic Review
Potential Molecular Mechanisms of Alzheimer’s Disease from Genetic Studies
by Martin Nwadiugwu, Hui Shen and Hong-Wen Deng
Biology 2023, 12(4), 602; https://doi.org/10.3390/biology12040602 - 15 Apr 2023
Cited by 2 | Viewed by 1891
Abstract
The devastating effects of Alzheimer’s disease (AD) are yet to be ameliorated due to the absence of curative treatment options. AD is an aging-related disease that affects cognition, and molecular imbalance is one of its hallmarks. There is a need to identify common [...] Read more.
The devastating effects of Alzheimer’s disease (AD) are yet to be ameliorated due to the absence of curative treatment options. AD is an aging-related disease that affects cognition, and molecular imbalance is one of its hallmarks. There is a need to identify common causes of molecular imbalance in AD and their potential mechanisms for continuing research. A narrative synthesis of molecular mechanisms in AD from primary studies that employed single-cell sequencing (scRNA-seq) or spatial genomics was conducted using Embase and PubMed databases. We found that differences in molecular mechanisms in AD could be grouped into four key categories: sex-specific features, early-onset features, aging, and immune system pathways. The reported causes of molecular imbalance were alterations in bile acid (BA) synthesis, PITRM1, TREM2, olfactory mucosa (OM) cells, cholesterol catabolism, NFkB, double-strand break (DSB) neuronal damage, P65KD silencing, tau and APOE expression. What changed from previous findings in contrast to results obtained were explored to find potential factors for AD-modifying investigations. Full article
(This article belongs to the Special Issue New Concepts in Brain Aging, Alzheimer's Disease and Related Dementias)
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