Special Issue "Dementia and Cognitive Ageing"

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

Deadline for manuscript submissions: 15 January 2020.

Special Issue Editors

Dr. Dorina Cadar
E-Mail Website
Guest Editor
UCL Department of Behavioural Science and Health, 1-19 Torrington Place, London, UK
Interests: dementia; cognitive impairment; neuropscyhological screening; lifestyle behaviours
Dr. Eddy J. Davelaar
E-Mail Website
Guest Editor
Department of Psychological Sciences, Birkbeck, University of London, Malet Street, London WC1E 7HX, UK
Interests: memory; cognitive training; cogntive decline

Special Issue Information

Dear Colleagues,

Dementia and cognitive impairment are not an inevitable part of the ageing process. To better understand the relationship between cognitive ageing and dementia, we pose the following questions: Why do some individuals have a faster than normal cognitive decline, leading to dementia, whereas others maintain good performance until the end of their life? There are many non-modifiable (e.g., genes) and modifiable (e.g., lifestyle) risk factors, but yet it remains unclear how they interact and whether they exert their influence during a critical age period of life (early, midlife, or early-later life). What is the evidence base for interventions targeting modifiable risk factors (e.g., diet, physical activity) offsetting the risk? What is the current state-of-the-art in behavioural or biological testing to identify people at risk of cognitive impairment and dementia?

In this Special Issue, we are seeking submissions that address some of the questions raised above. We aim to bring together new research from different fields, such as epidemiology, neurobiology, and neuropsychology to provide a multidisciplinary evidence base.

Thus, we are inviting research articles, reviews, and commentaries on a broad range of cognitive ageing and dementia research from observational, experimental and clinical studies.

Dr. Dorina Cadar
Dr. Eddy J. Davelaar
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 papers will be 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 1400 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

  • cognitive ageing
  • dementia
  • neuropscyhological screening
  • modifiable risk factors

Published Papers (5 papers)

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Open AccessArticle
An Investigation of Limbs Exercise as a Treatment in Improving the Psychomotor Speed in Older Adults with Mild Cognitive Impairment
Brain Sci. 2019, 9(10), 277; https://doi.org/10.3390/brainsci9100277 - 16 Oct 2019
Abstract
Objectives: This study investigated the effects of therapeutic structured limb exercises intended to improve psychomotor speed in older adults with mild cognitive impairment (MCI). Methods: Forty-four patients with mild cognitive impairment who met the inclusion criteria were selected and assigned randomly to either [...] Read more.
Objectives: This study investigated the effects of therapeutic structured limb exercises intended to improve psychomotor speed in older adults with mild cognitive impairment (MCI). Methods: Forty-four patients with mild cognitive impairment who met the inclusion criteria were selected and assigned randomly to either an experimental group (22 patients) or a control group (22 patients). The numbers of participants were selected based on the calculated sample effect size (N = 38). The study involved a 10-week intervention, in which participants completed structured limb exercises during 60-min training sessions delivered three times per week. Forty-one subjects completed the experimental programme. Scores in the Finger Tapping Test (FTT), Purdue Pegboard Test (PPT) and Montreal Cognitive Assessment (MoCA), along with electroencephalography (EEG) data, were collected before, during and after the intervention. The experimental and control groups were compared using repeated measures analysis of variance. Results: The patients with MCI in the experimental group achieved significantly improved scores in the FTT, the PPT and all dimensions of the MoCA. Moreover, these patients exhibited significant increases in the alpha and beta EEG wave power values in all brain areas of MCI patients, indicating that limb exercise training positively influenced their brain functions. Conclusions: The results conclude that a structured therapeutic limb exercise intervention can effectively improve psychomotor speed in patients with MCI and mitigate declines in cognitive function. This training intervention appears to be effective as a treatment for community-dwelling patients with MCI. Full article
(This article belongs to the Special Issue Dementia and Cognitive Ageing)
Open AccessArticle
A Deep Learning approach for Diagnosis of Mild Cognitive Impairment Based on MRI Images
Brain Sci. 2019, 9(9), 217; https://doi.org/10.3390/brainsci9090217 - 28 Aug 2019
Abstract
Mild cognitive impairment (MCI) is an intermediary stage condition between healthy people and Alzheimer’s disease (AD) patients and other dementias. AD is a progressive and irreversible neurodegenerative disorder, which is a significant threat to people, age 65 and older. Although MCI does not [...] Read more.
Mild cognitive impairment (MCI) is an intermediary stage condition between healthy people and Alzheimer’s disease (AD) patients and other dementias. AD is a progressive and irreversible neurodegenerative disorder, which is a significant threat to people, age 65 and older. Although MCI does not always lead to AD, an early diagnosis at the stage of MCI can be very helpful in identifying people who are at risk of AD. Moreover, the early diagnosis of MCI can lead to more effective treatment, or at least, significantly delay the disease’s progress, and can lead to social and financial benefits. Magnetic resonance imaging (MRI), which has become a significant tool for the diagnosis of MCI and AD, can provide neuropsychological data for analyzing the variance in brain structure and function. MCI is divided into early and late MCI (EMCI and LMCI) and sadly, there is no clear differentiation between the brain structure of healthy people and MCI patients, especially in the EMCI stage. This paper aims to use a deep learning approach, which is one of the most powerful branches of machine learning, to discriminate between healthy people and the two types of MCI groups based on MRI results. The convolutional neural network (CNN) with an efficient architecture was used to extract high-quality features from MRIs to classify people into healthy, EMCI, or LMCI groups. The MRIs of 600 individuals used in this study included 200 control normal (CN) people, 200 EMCI patients, and 200 LMCI patients. This study randomly selected 70 percent of the data to train our model and 30 percent for the test set. The results showed the best overall classification between CN and LMCI groups in the sagittal view with an accuracy of 94.54 percent. In addition, 93.96 percent and 93.00 percent accuracy were reached for the pairs of EMCI/LMCI and CN/EMCI, respectively. Full article
(This article belongs to the Special Issue Dementia and Cognitive Ageing)
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Open AccessArticle
Relation of Serum Plasmalogens and APOE Genotype to Cognition and Dementia in Older Persons in a Cross-Sectional Study
Brain Sci. 2019, 9(4), 92; https://doi.org/10.3390/brainsci9040092 - 24 Apr 2019
Abstract
Using a community sample of 1205 elderly persons, we investigated the associations and potential interactions between Apolipoprotein E (APOE) genotype and serum phosphatidylethanolamine (PlsEtn) on cognition and dementia. For each person, APOE genotype, PlsEtn Biosynthesis value (PBV, the combination of three key [...] Read more.
Using a community sample of 1205 elderly persons, we investigated the associations and potential interactions between Apolipoprotein E (APOE) genotype and serum phosphatidylethanolamine (PlsEtn) on cognition and dementia. For each person, APOE genotype, PlsEtn Biosynthesis value (PBV, the combination of three key PlsEtn species), cognition (the combination of five specific cognitive domains), and diagnosis of dementia was determined. APOE genotype and PBV were observed to be non-interacting (p > 0.05) and independently associated with cognition: APOE (relative to ε3ε3:ε2ε3 (Coef = 0.14, p = 4.2 × 10−2); ε3ε4/ε4ε4 (Coef = −0.22, p = 6.2 × 10−5); PBV (Coef = 0.12, p = 1.7 × 10−7) and dementia: APOE (relative to ε3ε3:ε2ε3 (Odds Ratio OR = 0.44, p = 3.0 × 10−2); ε3ε4/ε4ε4 (OR = 2.1, p = 2.2 × 10−4)); PBV (OR = 0.61, p = 3.3 × 10−6). Associations are expressed per standard deviation (SD) and adjusted for serum lipids and demographics. Due to the independent and non-interacting nature of the APOE and PBV associations, the prevalence of dementia in APOE ε3ε4/ε4ε4 persons with high PBV values (>1 SD from mean) was observed to be the same as APOE ε3ε3 persons (14.3% versus 14.0%). Similarly, the prevalence of dementia in APOE ε3ε3 persons with high PBV values was only 5.7% versus 6.7% for APOE ε2ε3 persons. The results of these analyses indicate that the net effect of APOE genotype on cognition and the prevalence of dementia is dependent upon the plasmalogen status of the person. Full article
(This article belongs to the Special Issue Dementia and Cognitive Ageing)
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Open AccessArticle
N-Acetyl Cysteine Supplement Minimize Tau Expression and Neuronal Loss in Animal Model of Alzheimer’s Disease
Brain Sci. 2018, 8(10), 185; https://doi.org/10.3390/brainsci8100185 - 11 Oct 2018
Cited by 2
Abstract
Alzheimer’s disease (AD) is characterized by the accumulation of neurofibrillary tangles (NFT), deposition of beta amyloid plaques, and consequent neuronal loss in the brain tissue. Oxidative stress to the neurons is often attributed to AD, but its link to NFT and β-amyloid protein [...] Read more.
Alzheimer’s disease (AD) is characterized by the accumulation of neurofibrillary tangles (NFT), deposition of beta amyloid plaques, and consequent neuronal loss in the brain tissue. Oxidative stress to the neurons is often attributed to AD, but its link to NFT and β-amyloid protein (BAP) still remains unclear. In an animal model of AD, we boosted the oxidative defense by N-Acetyl cysteine (NAC), a precursor of glutathione, a powerful antioxidant and free radical scavenger, to understand the link between oxidative stress and NFT. In mimicking AD, intracerebroventricular (ICV) colchicine, a microtubule disrupting agent also known to cause oxidative stress was administered to the rats. The animal groups consisted of an age-matched control, sham operated, AD, and NAC treated in AD models of rats. Cognitive function was evaluated in a passive avoidance test; neuronal degeneration was quantified using Nissl staining. NFT in the form of abnormal tau expression in different regions of the brain were evaluated through immunohistochemistry using rabbit anti-tau antibody. ICV has resulted in significant cognitive and neuronal loss in medial prefrontal cortex (MFC) and all the regions of the hippocampus. It has also resulted in increased accumulation of intraneuronal tau in the hippocampus and MFC. NAC treatment in AD model rats has reversed the cognitive loss and neuronal degeneration. The intraneuronal tau expression also minimized with NAC treatment in AD model rats. Thus, our findings suggest that an antioxidant supplement during the progression of AD is likely to prevent neuronal degeneration by minimizing the neurofibrillary degeneration in the form of tau accumulation. Full article
(This article belongs to the Special Issue Dementia and Cognitive Ageing)
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Open AccessPerspective
An Overview of Experimental and Clinical Spinal Cord Findings in Alzheimer’s Disease
Brain Sci. 2019, 9(7), 168; https://doi.org/10.3390/brainsci9070168 - 17 Jul 2019
Abstract
Alzheimer’s disease (AD) is a neurodegenerative disorder that occurs mainly in the elderly and presenile life stages. It is estimated that by the year 2050, 135 million people will be affected by AD worldwide, representing a huge burden to society. The pathological hallmarks [...] Read more.
Alzheimer’s disease (AD) is a neurodegenerative disorder that occurs mainly in the elderly and presenile life stages. It is estimated that by the year 2050, 135 million people will be affected by AD worldwide, representing a huge burden to society. The pathological hallmarks of AD mainly include intracellular neurofibrillary tangles (NFTs) caused by hyperphosphorylation of tau protein, formation of extracellular amyloid plaques, and massive neural cell death in the affected nervous system. The pathogenesis of AD is very complicated, and recent scientific research on AD is mainly concentrated on the cortex and hippocampus. Although the spinal cord is a pivotal part of the central nervous system, there are a limited number of studies focusing on the spinal cord. As an extension of the brain, the spinal cord functions as the bridge between the brain and various parts of the body. However, pathological changes in the spinal cord in AD have not been comprehensively and systematically studied at present. We here review the existing progress on the pathological features of AD in the spinal cord. Full article
(This article belongs to the Special Issue Dementia and Cognitive Ageing)
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