Over time, the body undergoes a natural, multifactorial, and ongoing process named senescence, which induces changes at the molecular, cellular, and micro-anatomical levels in many body systems. The brain, being a highly complex organ, is particularly affected by this process, potentially impairing its numerous functions. The brain relies on chemical messengers known as neurotransmitters to function properly, with dopamine being one of the most crucial. This catecholamine is responsible for a broad range of critical roles in the central nervous system, including movement, learning, cognition, motivation, emotion, reward, hormonal release, memory consolidation, visual performance, sexual drive, modulation of circadian rhythms, and brain development. In the present review, we thoroughly examine the impact of senescence on the dopaminergic system, with a primary focus on the classic delimitations of the dopaminergic nuclei from A8 to A17. We provide in-depth information about their anatomy and function, particularly addressing how senescence affects each of these nuclei.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.jchemneu.2024.102415 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by motor and non-motor symptoms, primarily due to the degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Factors contributing to this neuronal degeneration include mitochondrial dysfunction, oxidative stress, and neuronal excitotoxicity. Despite extensive research, the exact etiology of PD remains unclear, with both genetic and environmental factors playing significant roles.
View Article and Find Full Text PDFGalantamine-Memantine Combination in the Treatment of Parkinson's Disease Dementia.
Brain Sci
November 2024
Department of Public Safety and Correctional Services, Baltimore, MD 21215, USA.
Parkinson's disease (PD) is a progressive neurodegenerative disorder that affects over 1% of population over age 60. It is defined by motor and nonmotor symptoms including a spectrum of cognitive impairments known as Parkinson's disease dementia (PDD). Currently, the only US Food and Drug Administration-approved treatment for PDD is rivastigmine, which inhibits acetylcholinesterase and butyrylcholinesterase increasing the level of acetylcholine in the brain.
View Article and Find Full Text PDFBehavioral analysis of motor and non-motor impairment in rodent models of Parkinson's disease.
Front Aging Neurosci
December 2024
CHU de Québec-Université Laval Research Center, Neuroscience Axis, Québec City, QC, Canada.
Parkinson's disease (PD) is a prevalent neurodegenerative disorder characterized by the degeneration of dopamine neurons in the substantia nigra pars compacta, leading to motor and non-motor symptoms. While motor symptoms such as rigidity, tremor, bradykinesia/akinesia, and postural instability are well-recognized, non-motor symptoms including cognitive decline, depression, and anxiety also significantly impact patients' quality of life. Preclinical research utilizing animal models has been instrumental in understanding PD pathophysiology and exploring therapeutic interventions.
View Article and Find Full Text PDFAging-related losses in dopamine D2/3 receptor availability are linked to working-memory decline across five years.
Cereb Cortex
January 2025
Aging Research Center, Karolinska Institutet and Stockholm University, Tomtebodavägen 18 A, SE-171 65 Solna, Sweden.
Although age differences in the dopamine system have been suggested to contribute to age-related cognitive decline based on cross-sectional data, recent large-scale cross-sectional studies reported only weak evidence for a correlation among aging, dopamine receptor availability, and cognition. Regardless, longitudinal data remain essential to make robust statements about dopamine losses as a basis for cognitive aging. We present correlations between changes in D2/3 dopamine receptor availability and changes in working memory measured over 5 yr in healthy, older adults (n = 128, ages 64 to 68 yr at baseline).
View Article and Find Full Text PDFPark7 deletion leads to sex-specific transcriptome changes involving NRF2-CYP1B1 axis in mouse midbrain astrocytes.
NPJ Parkinsons Dis
January 2025
Department of Life Sciences and Medicine (DLSM), University of Luxembourg, Belvaux, Luxembourg.
Loss-of-function mutations in PARK7, encoding for DJ-1, can lead to early onset Parkinson's disease (PD). In mice, Park7 deletion leads to dopaminergic deficits during aging, and increased sensitivity to oxidative stress. However, the severity of the reported phenotypes varies.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!