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Ageing and Neurodegeneration in the Retina and Brain
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Ageing and Neurodegeneration in the Retina and Brain

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Clinical Neurology".

Deadline for manuscript submissions: closed (31 March 2019)

Special Issue Editor

Prof. Dr. M. Francesca Cordeiro

E-Mail Website
Guest Editor
Professor & Chair of Ophthalmology Imperial College London, Imperial College Ophthalmology Research Group Clinical Trials Unit Director, UCL Professor of Retinal Neurodegeneration & Glaucoma Studies, Hon. Consultant Ophthalmologist Western Eye Hospital, London, UK
Interests: neurodegeneration; glaucoma; ageing; apoptosis; neuroprotection

Special Issue Information

Dear Colleagues,

The ageing of the central nervous system is a ubiquitous phenomenon that will impact the majority of people during their lifetime. Improvements in cardiovascular health and living standards have boosted life expectancy at a rate surpassing our discovery of ways in which to protect the central nervous system against involution, thus impacting quality of later life in many ways. In order to combat this, we are advancing brain imaging and the use of emerging surrogate markers in order to quantify and study the rate of age-related neuronal loss in vivo. One such potential method involves using the retina as a directly visible extension of the central nervous system, permitted due to high resolution images attainable through the clear optical media of the eye.

In this Special Issue, we include the latest overviews of studies both in animals and humans that are leading towards novel investigations and treatments targeting the ageing process. Using a range of techniques and models, it has been possible to identify several biochemical targets for neuroprotective therapies that have shown promising results in animals. The challenge of translating this into humans begins with the inherent difficulties of studying diseases of slow progression, multiple risk factors and poorly understood or reproducible biomarkers. Thus the next decade in this field is an exciting area with much to learn and discover.

Prof. Dr. M. Francesca Cordeiro
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. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly 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 2600 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
  • Ageing
  • Brain
  • Retina
  • Glaucoma
  • Alzheimer's disease
  • Parkinson's disease
  • Dementia
  • Apoptosis
  • Neuroprotection

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

Published Papers (2 papers)

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Review

23 pages, 2430 KiB  
Review
Newly Generated and Non-Newly Generated “Immature” Neurons in the Mammalian Brain: A Possible Reservoir of Young Cells to Prevent Brain Aging and Disease?
by Chiara La Rosa, Marco Ghibaudi and Luca Bonfanti
J. Clin. Med. 2019, 8(5), 685; https://doi.org/10.3390/jcm8050685 - 15 May 2019
Cited by 33 | Viewed by 6720
Abstract
Brain plasticity is important for translational purposes since most neurological disorders and brain aging problems remain substantially incurable. In the mammalian nervous system, neurons are mostly not renewed throughout life and cannot be replaced. In humans, the increasing life expectancy explains the increase [...] Read more.
Brain plasticity is important for translational purposes since most neurological disorders and brain aging problems remain substantially incurable. In the mammalian nervous system, neurons are mostly not renewed throughout life and cannot be replaced. In humans, the increasing life expectancy explains the increase in brain health problems, also producing heavy social and economic burden. An exception to the “static” brain is represented by stem cell niches leading to the production of new neurons. Such adult neurogenesis is dramatically reduced from fish to mammals, and in large-brained mammals with respect to rodents. Some examples of neurogenesis occurring outside the neurogenic niches have been reported, yet these new neurons actually do not integrate in the mature nervous tissue. Non-newly generated, “immature” neurons (nng-INs) are also present: Prenatally generated cells continuing to express molecules of immaturity (mostly shared with the newly born neurons). Of interest, nng-INs seem to show an inverse phylogenetic trend across mammals, being abundant in higher-order brain regions not served by neurogenesis and providing structural plasticity in rather stable areas. Both newly generated and nng-INs represent a potential reservoir of young cells (a “brain reserve”) that might be exploited for preventing the damage of aging and/or delay the onset/reduce the impact of neurological disorders. Full article
(This article belongs to the Special Issue Ageing and Neurodegeneration in the Retina and Brain)
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Graphical abstract

57 pages, 1245 KiB  
Review
Vascular Dysfunction in Alzheimer’s Disease: A Prelude to the Pathological Process or a Consequence of It?
by Karan Govindpani, Laura G McNamara, Nicholas R Smith, Chitra Vinnakota, Henry J Waldvogel, Richard LM Faull and Andrea Kwakowsky
J. Clin. Med. 2019, 8(5), 651; https://doi.org/10.3390/jcm8050651 - 10 May 2019
Cited by 171 | Viewed by 11796
Abstract
Alzheimer’s disease (AD) is the most prevalent form of dementia. Despite decades of research following several theoretical and clinical lines, all existing treatments for the disorder are purely symptomatic. AD research has traditionally been focused on neuronal and glial dysfunction. Although there is [...] Read more.
Alzheimer’s disease (AD) is the most prevalent form of dementia. Despite decades of research following several theoretical and clinical lines, all existing treatments for the disorder are purely symptomatic. AD research has traditionally been focused on neuronal and glial dysfunction. Although there is a wealth of evidence pointing to a significant vascular component in the disease, this angle has been relatively poorly explored. In this review, we consider the various aspects of vascular dysfunction in AD, which has a significant impact on brain metabolism and homeostasis and the clearance of β-amyloid and other toxic metabolites. This may potentially precede the onset of the hallmark pathophysiological and cognitive symptoms of the disease. Pathological changes in vessel haemodynamics, angiogenesis, vascular cell function, vascular coverage, blood-brain barrier permeability and immune cell migration may be related to amyloid toxicity, oxidative stress and apolipoprotein E (APOE) genotype. These vascular deficits may in turn contribute to parenchymal amyloid deposition, neurotoxicity, glial activation and metabolic dysfunction in multiple cell types. A vicious feedback cycle ensues, with progressively worsening neuronal and vascular pathology through the course of the disease. Thus, a better appreciation for the importance of vascular dysfunction in AD may open new avenues for research and therapy. Full article
(This article belongs to the Special Issue Ageing and Neurodegeneration in the Retina and Brain)
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