Neuronal plasticity, the brain's ability to adapt structurally and functionally, Is essential for learning, memory, and recovery from injuries. In neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease, this plasticity is disrupted, leading to cognitive and motor deficits. This review explores the mechanisms of neuronal plasticity and its effect on Alzheimer's disease and Parkinson's disease. Alzheimer's disease features amyloid-beta plaques and tau tangles that impair synaptic function, while Parkinson's disease involves the loss of dopaminergic neurons affecting motor control. Enhancing neuronal plasticity offers therapeutic potential for these diseases. A systematic literature review was conducted using databases such as PubMed, Scopus, and Google Scholar, focusing on studies of neuronal plasticity in Alzheimer's disease and Parkinson's disease. Data synthesis identified key themes such as synaptic mechanisms, neurogenesis, and therapeutic strategies, linking molecular insights to clinical applications. Results highlight that targeting synaptic plasticity mechanisms, such as long-term potentiation and long-term depression, shows promise. Neurotrophic factors, advanced imaging techniques, and molecular tools (e.g., clustered regularly interspaced short palindromic repeats and optogenetics) are crucial in understanding and enhancing plasticity. Current therapies, including dopamine replacement, deep brain stimulation, and lifestyle interventions, demonstrate the potential to alleviate symptoms and improve outcomes. In conclusion, enhancing neuronal plasticity through targeted therapies holds significant promise for treating neurodegenerative diseases. Future research should integrate multidisciplinary approaches to fully harness the therapeutic potential of neuronal plasticity in Alzheimer's disease and Parkinson's disease.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.4103/NRR.NRR-D-24-01019 | DOI Listing |
Neural Plast
December 2024
Department of Psychology, Sigmund Freud University, Milan, Italy.
The phenomenon of neural plasticity pertains to the intrinsic capacity of neurons to undergo structural and functional reconfiguration through learning and experiential interaction with the environment. These changes could manifest themselves not only as a consequence of various life experiences but also following therapeutic interventions, including the application of noninvasive brain stimulation (NIBS) and psychotherapy. As standalone therapies, both NIBS and psychotherapy have demonstrated their efficacy in the amelioration of psychiatric disorders' symptoms, with a certain variability in terms of effect sizes and duration.
View Article and Find Full Text PDFAm J Chin Med
December 2024
Heilongjiang University of Chinese Medicine, Harbin, Heilongjiang 150040, P. R. China.
Alzheimer's disease (AD), the predominant form of dementia, is a neurodegenerative disorder of the central nervous system (CNS) characterized by a subtle onset and a spectrum of cognitive and functional declines. The clinical manifestation of AD encompasses memory deficits, cognitive deterioration, and behavioral disturbances, culminating in a severe impairment of daily living skills. Despite its high prevalence, accounting for 60-70% of all dementia cases, there remains an absence of curative therapeutics.
View Article and Find Full Text PDFCurr Opin Neurobiol
December 2024
Department of Pharmacology, University of Colorado School of Medicine, Anschutz Medical Campus, 12800 East 19th Avenue, Aurora, CO 80045, USA. Electronic address:
GABAergic synaptic inhibition controls circuit function by regulating neuronal plasticity, excitability, and firing. To achieve these goals, inhibitory synapses themselves undergo several forms of plasticity via diverse mechanisms, strengthening and weakening phasic inhibition in response to numerous activity-induced stimuli. These mechanisms include changing the number and arrangement of functional GABARs within the inhibitory postsynaptic domain (iPSD), which can profoundly regulate inhibitory synapse strength.
View Article and Find Full Text PDFRedox Biol
December 2024
Baruch College and CUNY Graduate Center, 1 Baruch Way, New York, NY, 10010, USA. Electronic address:
The elevated emission of reactive oxygen species (ROS) from presynaptic mitochondria is well-documented in several inflammatory and neurodegenerative diseases. However, the potential role of mitochondrial ROS in presynaptic function and plasticity remains largely understudied beyond the context of disease. Here, we investigated this potential ROS role in presynaptic function and short-term plasticity by combining optogenetics, whole cell electrophysiological recordings, and live confocal imaging using a well-established protocol for induction and measurement of synaptic potentiation in Drosophila melanogaster neuromuscular junctions (NMJ).
View Article and Find Full Text PDFHum Brain Mapp
December 2024
Institute of Cognitive Neuroscience, Department of Biopsychology, Faculty of Psychology, Ruhr University Bochum, Bochum, Germany.
Learning new categories is fundamental to cognition, occurring in daily life through various sensory modalities. However, it is not well known how acquiring new categories can modulate the brain networks. Resting-state functional connectivity is an effective method for detecting short-term brain alterations induced by various modality-based learning experiences.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!