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Genetics and Genomics of Aging and Dementia
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Genetics and Genomics of Aging and Dementia

A special issue of Genes (ISSN 2073-4425). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (20 October 2023) | Viewed by 2828

Special Issue Editors

Prof. Dr. Teresa Juárez-Cedillo

E-Mail Website
Guest Editor
Instituto Mexicano del Seguro Social, Avenida Cuauhtémoc No. 330, Col. Doctores, Delegación Cuauhtémoc, México D.F. C.P. 06725, Mexico
Interests: genetics; geriatrics; dementia; cognitive decline; pharmacoepidemiology; pharmacogenetics; geriatrics
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Alfredo Ramirez

E-Mail Website
Guest Editor
Department of Psychiatry and Psychotherapy, Medical Faculty, University of Cologne, 50931 Cologne, Germany
Interests: genetics; genetic epidemiology; geriatrics; psychiatry

Special Issue Information

Dear Colleagues,

The study of genetic information on the biological mechanisms involved in cognitive decline has become increasingly relevant and received much attention in recent years, focusing the search for new genetic biomarkers that allow early diagnosis and in turn characterize the population at risk of developing some type of neurological disease that occurs with aging.

Dementia is characterized by severe memory loss and cognitive impairment, resulting in complete dependency and reduced life expectancy. Genetic studies have shown us that some genetic variants have linked both haplogroups and mitochondrial variants with the development of aging and the chronic diseases that characterize it, such as dementia. In addition to some polymorphisms, mutations, and haplogroups, there is another risk factor that plays an important role in the regulation, development, and prognosis of chronic-degenerative diseases such as Alzheimer's and other dementias.

In this Special Issue, we would like to invite submissions of original research or review articles on topics relevant to "Genetics and Genomics of Aging and Dementia". We hope to contribute to the knowledge of the genetic mechanisms involved in aging that trigger cognitive decline and lead us to dementia to propose new therapeutic strategies that allow maintaining the functionality of populations. We look forward to receiving your contributions.

Prof. Dr. Teresa Juárez-Cedillo
Prof. Dr. Alfredo Ramirez
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. Genes 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 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.

Published Papers (2 papers)

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Research

18 pages, 3505 KiB  
Article
Behavioral and Neuronal Characterizations, across Ages, of the TgSwDI Mouse Model of Alzheimer’s Disease
by Natalie A. Tan, Angelica M. Alvarado Carpio, H. Craig Heller and Elsa C. Pittaras
Genes 2024, 15(1), 47; https://doi.org/10.3390/genes15010047 - 28 Dec 2023
Viewed by 893
Abstract
Alzheimer’s disease (AD) is a neurodegenerative disorder that currently affects as many as 50 million people worldwide. It is neurochemically characterized by an aggregation of β-amyloid plaques and tau neurofibrillary tangles that result in neuronal dysfunction, cognitive decline, and a progressive loss of [...] Read more.
Alzheimer’s disease (AD) is a neurodegenerative disorder that currently affects as many as 50 million people worldwide. It is neurochemically characterized by an aggregation of β-amyloid plaques and tau neurofibrillary tangles that result in neuronal dysfunction, cognitive decline, and a progressive loss of brain function. TgSwDI is a well-studied transgenic mouse model of AD, but no longitudinal studies have been performed to characterize cognitive deficits or β-amyloid plaque accumulation for use as a baseline reference in future research. Thus, we use behavioral tests (T-Maze, Novel Object Recognition (NOR), Novel Object Location (NOL)) to study long-term and working memory, and immunostaining to study β-amyloid plaque deposits, as well as brain size, in hippocampal, cerebellum, and cortical slices in TgSwDI and wild-type (WT) mice at 3, 5, 8, and 12 months old. The behavioral results show that TgSwDI mice exhibit deficits in their long-term spatial memory starting at 8 months old and in long-term recognition memory at all ages, but no deficits in their working memory. Immunohistochemistry showed an exponential increase in β-amyloid plaque in the hippocampus and cortex of TgSwDI mice over time, whereas there was no significant accumulation of plaque in WT mice at any age. Staining showed a smaller hippocampus and cerebellum starting at 8 months old for the TgSwDI compared to WT mice. Our data show how TgSwDI mice differ from WT mice in their baseline levels of cognitive function and β-amyloid plaque load throughout their lives. Full article
(This article belongs to the Special Issue Genetics and Genomics of Aging and Dementia)
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14 pages, 2604 KiB  
Article
Longitudinal Changes in Mitochondrial DNA Copy Number and Telomere Length in Patients with Parkinson’s Disease
by Alberto Ortega-Vázquez, Salvador Sánchez-Badajos, Miguel Ángel Ramírez-García, Diana Alvarez-Luquín, Marisol López-López, Laura Virginia Adalid-Peralta and Nancy Monroy-Jaramillo
Genes 2023, 14(10), 1913; https://doi.org/10.3390/genes14101913 - 07 Oct 2023
Cited by 2 | Viewed by 1096
Abstract
Parkinson’s disease (PD) pathophysiology includes mitochondrial dysfunction, neuroinflammation, and aging as its biggest risk factors. Mitochondrial DNA copy number (mtDNA-CN) and telomere length (TL) are biological aging markers with inconclusive results regarding their association with PD. A case–control study was used to measure [...] Read more.
Parkinson’s disease (PD) pathophysiology includes mitochondrial dysfunction, neuroinflammation, and aging as its biggest risk factors. Mitochondrial DNA copy number (mtDNA-CN) and telomere length (TL) are biological aging markers with inconclusive results regarding their association with PD. A case–control study was used to measure TL and mtDNA-CN using qPCR in PBMCs. PD patients were naive at baseline (T0) and followed-up at one (T1) and two (T2) years after the dopaminergic treatment (DRT). Plasmatic cytokines were determined by ELISA in all participants, along with clinical parameters of patients at T0. While TL was shorter in patients vs. controls at all time points evaluated (p < 0.01), mtDNA-CN showed no differences. An increase in mtDNA-CN and TL was observed in treated patients vs. naive ones (p < 0.001). Our statistical model analyzed both aging markers with covariates, showing a strong correlation between them (r = 0.57, p < 0.01), and IL-17A levels positively correlating with mtDNA-CN only in untreated patients (r = 0.45, p < 0.05). TL and mtDNA-CN could be useful markers for monitoring inflammation progression or treatment response in PD. DRT might modulate TL and mtDNA-CN, reflecting a compensatory mechanism to counteract mitochondrial dysfunction in PD, but this needs further investigation. Full article
(This article belongs to the Special Issue Genetics and Genomics of Aging and Dementia)
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