Mitochondrial dysfunction caused by mitochondrial DNA (mtDNA) aberrations has been implicated in the neuronal death in neurodegenerative disorders. Significant neuronal damage can occur if the percentage of mtDNA mutations may reach a critical threshold. mtDNA mutations also accumulate during normal aging. Here we quantified the 5 kB common mtDNA deletion (CD) using real-time PCR in various brain regions from neurodegenerative disorders and controls. We confirmed previous results that the CD levels increase with age, reaching highest levels in the basal ganglia. High CD levels were also found in affected regions in frontotemporal dementia, Parkinson's disease, and dementia with Lewy bodies, but not in Alzheimer's disease. This suggests that mtDNA damage may occur in a region-specific distribution in neurodegenerative disorders.
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http://dx.doi.org/10.1016/j.neulet.2003.11.073 | DOI Listing |
Curr Top Med Chem
January 2025
Graphic Era (Deemed to be University), Clement Town Dehradun, India.
Alzheimer's Disease (AD), a progressive neurodegenerative disorder, is characterized by the accumulation of neurofibrillary tangles and β-amyloid plaques, leading to a decline in cognitive function. AD is characterized by tau protein hyperphosphorylation and extracellular β-amyloid accumulation. Even after much research, there are still no proven cures for AD.
View Article and Find Full Text PDFCurr Treat Options Neurol
July 2024
Department of Neurology, Division of Behavioral Neurology, Stanford Neuroscience Health Center, 453 Quarry Road, Palo Alto, CA 94304, USA.
Purpose Of Review: The purpose of this review is to discuss the clinical, radiological, and neuropathological heterogeneity of corticobasal syndrome (CBS), which can complicate the determination of underlying etiology and lead to inaccurate treatment decisions. Though the most common diagnosis is corticobasal degeneration (CBD), the spectrum of underlying pathologies expands beyond CBD and can overlap with other neurodegenerative diseases and even the neuroimmunology field. We will review possible clinical presentations and cues that can point towards the etiology.
View Article and Find Full Text PDFAlzheimers Dement (Amst)
January 2025
Weill Institute for Neurosciences, Department of Neurology, Memory and Aging Center University of California, San Francisco San Francisco California USA.
Introduction: Plasma amyloid beta/amyloid beta (Aβ/Aβ) and phosphorylated tau217 (p-tau217) identify individuals with primary Alzheimer's disease (AD). They may detect AD co-pathology in the setting of other primary neurodegenerative diseases, but this has not been systematically studied.
Methods: We compared the clinical, neuroimaging, and neuropathological associations of plasma Aβ/Aβ (mass spectrometry), p-tau217 (electrochemiluminescence), and neurofilament light ([NfL], single molecule array [Simoa]), as markers of AD co-pathology, in a sporadic frontotemporal dementia (FTD) cohort ( = 620).
Introduction: Clinicopathological correlations differ by sex in Lewy body dementia (LBD). However, previous studies have focused on pathological staging systems that place less emphasis on regional pathologies.
Methods: We included 357 people (131 female, 226 male) with a high likelihood of LBD based on pathology from the Brain Bank for Neurodegenerative (Jacksonville, FL).
Alzheimers Dement (Amst)
January 2025
Introduction: Brain age gap (BAG), defined as the difference between MRI-predicted 'brain age' and chronological age, can capture information underlying various neurological disorders. We investigated the pathophysiological significance of the BAG across neurodegenerative disorders.
Methods: We developed a brain age estimator using structural MRIs of healthy-aged individuals from one cohort study.
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