Here we isolated and characterized the complete mitochondrial genome of the hybrid grouper (♀ × ♂). It is 16,503 bp long and contains 13 protein-coding genes, 2 rRNA genes, 22 tRNA genes, and a control region. The nucleotide composition is 29.08% of A, 29.03% of C, 15.66% of G and 26.23% of T, with 55.31% A + T. The phylogenetic analysis by neighbor-joining (NJ) method reveals that the hybrid offspring has a closer relationship to .
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http://dx.doi.org/10.1080/23802359.2021.1899071 | DOI Listing |
Alzheimers Dement
December 2024
Translational Gerontology Branch, National Institute on Aging, NIH, Baltimore, MD, USA.
Background: The mitochondrial cascade hypothesis suggests that mitochondrial dysfunction plays an important role in the pathogenesis of Alzheimer's disease dementia. Recent data have shown that mitochondrial DNA copy number (mtDNAcn) in human blood is associated with dementia risk and cognitive function, but which specific cognitive measures or domains are associated with mitochondrial dysfunction and whether this relationship is affected by health deterioration such as physical frailty or mitochondrial somatic mutations is not clear.
Methods: We measured mtDNAcn and heteroplasmies using fastMitoCalc and MitoCaller, respectively, from UK Biobank Whole Genome Sequencing (WGS) data at study entry (2006-2010).
Alzheimers Dement
December 2024
University of Kansas Medical Center, Kansas City, KS, USA.
Background: Alzheimer's disease (AD) pathology begins decades before clinical onset of dementia. Amyloid beta (Aβ) generally accumulates first in cognitively normal (ND) individuals, with tau and cognitive abnormalities following. AD pathologies have been found to correlate and interact with metabolic and mitochondrial outcomes in studies spanning numerous experimental paradigms.
View Article and Find Full Text PDFBackground: Alzheimer's disease is characterized by early decreases in cerebral glucose metabolism which are linked to reduced glucose transporter 1 (GLUT1) expression at the blood-brain barrier (BBB). Another key disease hallmark is the abundance of Aβ peptides as plaques in the brain which arise from the processing of the amyloid precursor protein (APP). Autosomal dominant inherited mutations causatively link APP itself to AD, rendering it imperative to fully understand APP's physiological functions to define the underlying biology of AD.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Keenan Research Centre for Biomedical Science, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, ON, Canada.
Background: Mild Cognitive Impairment (MCI) is often a precursor to Alzheimer's dementia (AD). Recent research underscores the relationship between mitochondrial dysfunction and amyloid-beta accumulation, raising the prospect of targeting mitochondrial function for intervention. Transcranial photobiomodulation (tPBM), a non-invasive technique utilizing near-infrared light, has been shown to enhance mitochondrial function.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Keenan Research Centre for Biomedical Science, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, ON, Canada.
Background: Mild Cognitive Impairment (MCI) serves as a precursor to Alzheimer's dementia (AD). Recent research underscores the relationship between mitochondrial dysfunction and amyloid beta accumulation, underscoring the prospect of targeting mitochondrial function for intervention. Consequently, our study aimed to explore the efficacy of transcranial photobiomodulation (tPBM), a novel non-invasive technique utilizing near-infrared light to activate mitochondrial cytochrome C oxidase receptors, thereby enhancing cellular energy in individuals with MCI.
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