Firing Alterations of Neurons in Alzheimer’s Disease: Are They Merely a Consequence of Pathogenesis or a Pivotal Component of Disease Progression?
Alzheimer’s disease (AD) is the most prevalent neurodegenerative disorder, yet its underlying causes remain elusive. The conventional perspective on disease pathogenesis attributes alterations in neuronal excitability to molecular changes resulting in synaptic dysfunction. Early hyperexcitability is...
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MDPI AG
2024-02-01
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| Online Access: | https://www.mdpi.com/2073-4409/13/5/434 |
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| author | Nikolaos P. Tzavellas Konstantinos I. Tsamis Andreas P. Katsenos Athena S. Davri Yannis V. Simos Ilias P. Nikas Stefanos Bellos Panagiotis Lekkas Foivos S. Kanellos Spyridon Konitsiotis Charalampos Labrakakis Patra Vezyraki Dimitrios Peschos |
| author_facet | Nikolaos P. Tzavellas Konstantinos I. Tsamis Andreas P. Katsenos Athena S. Davri Yannis V. Simos Ilias P. Nikas Stefanos Bellos Panagiotis Lekkas Foivos S. Kanellos Spyridon Konitsiotis Charalampos Labrakakis Patra Vezyraki Dimitrios Peschos |
| author_sort | Nikolaos P. Tzavellas |
| collection | DOAJ |
| description | Alzheimer’s disease (AD) is the most prevalent neurodegenerative disorder, yet its underlying causes remain elusive. The conventional perspective on disease pathogenesis attributes alterations in neuronal excitability to molecular changes resulting in synaptic dysfunction. Early hyperexcitability is succeeded by a progressive cessation of electrical activity in neurons, with amyloid beta (Aβ) oligomers and tau protein hyperphosphorylation identified as the initial events leading to hyperactivity. In addition to these key proteins, voltage-gated sodium and potassium channels play a decisive role in the altered electrical properties of neurons in AD. Impaired synaptic function and reduced neuronal plasticity contribute to a vicious cycle, resulting in a reduction in the number of synapses and synaptic proteins, impacting their transportation inside the neuron. An understanding of these neurophysiological alterations, combined with abnormalities in the morphology of brain cells, emerges as a crucial avenue for new treatment investigations. This review aims to delve into the detailed exploration of electrical neuronal alterations observed in different AD models affecting single neurons and neuronal networks. |
| first_indexed | 2024-04-25T00:33:22Z |
| format | Article |
| id | doaj.art-6729a928487d42e69274516b192c8ad8 |
| institution | Directory Open Access Journal |
| issn | 2073-4409 |
| language | English |
| last_indexed | 2024-04-25T00:33:22Z |
| publishDate | 2024-02-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | Cells |
| spelling | doaj.art-6729a928487d42e69274516b192c8ad82024-03-12T16:41:42ZengMDPI AGCells2073-44092024-02-0113543410.3390/cells13050434Firing Alterations of Neurons in Alzheimer’s Disease: Are They Merely a Consequence of Pathogenesis or a Pivotal Component of Disease Progression?Nikolaos P. Tzavellas0Konstantinos I. Tsamis1Andreas P. Katsenos2Athena S. Davri3Yannis V. Simos4Ilias P. Nikas5Stefanos Bellos6Panagiotis Lekkas7Foivos S. Kanellos8Spyridon Konitsiotis9Charalampos Labrakakis10Patra Vezyraki11Dimitrios Peschos12Department of Physiology, Faculty of Medicine, School of Health Sciences, University of Ioannina, 451 10 Ioannina, GreeceDepartment of Physiology, Faculty of Medicine, School of Health Sciences, University of Ioannina, 451 10 Ioannina, GreeceDepartment of Physiology, Faculty of Medicine, School of Health Sciences, University of Ioannina, 451 10 Ioannina, GreeceDepartment of Physiology, Faculty of Medicine, School of Health Sciences, University of Ioannina, 451 10 Ioannina, GreeceDepartment of Physiology, Faculty of Medicine, School of Health Sciences, University of Ioannina, 451 10 Ioannina, GreeceMedical School, University of Cyprus, 2029 Nicosia, CyprusDepartment of Physiology, Faculty of Medicine, School of Health Sciences, University of Ioannina, 451 10 Ioannina, GreeceDepartment of Physiology, Faculty of Medicine, School of Health Sciences, University of Ioannina, 451 10 Ioannina, GreeceDepartment of Physiology, Faculty of Medicine, School of Health Sciences, University of Ioannina, 451 10 Ioannina, GreeceDepartment of Neurology, Faculty of Medicine, School of Health Sciences, University Hospital of Ioannina, 455 00 Ioannina, GreeceDepartment of Biological Applications and Technology, University of Ioannina, 451 10 Ioannina, GreeceDepartment of Physiology, Faculty of Medicine, School of Health Sciences, University of Ioannina, 451 10 Ioannina, GreeceDepartment of Physiology, Faculty of Medicine, School of Health Sciences, University of Ioannina, 451 10 Ioannina, GreeceAlzheimer’s disease (AD) is the most prevalent neurodegenerative disorder, yet its underlying causes remain elusive. The conventional perspective on disease pathogenesis attributes alterations in neuronal excitability to molecular changes resulting in synaptic dysfunction. Early hyperexcitability is succeeded by a progressive cessation of electrical activity in neurons, with amyloid beta (Aβ) oligomers and tau protein hyperphosphorylation identified as the initial events leading to hyperactivity. In addition to these key proteins, voltage-gated sodium and potassium channels play a decisive role in the altered electrical properties of neurons in AD. Impaired synaptic function and reduced neuronal plasticity contribute to a vicious cycle, resulting in a reduction in the number of synapses and synaptic proteins, impacting their transportation inside the neuron. An understanding of these neurophysiological alterations, combined with abnormalities in the morphology of brain cells, emerges as a crucial avenue for new treatment investigations. This review aims to delve into the detailed exploration of electrical neuronal alterations observed in different AD models affecting single neurons and neuronal networks.https://www.mdpi.com/2073-4409/13/5/434Alzheimer’s diseaseneurophysiologypyramidal neuronsinterneuronsLTPdendritic spine |
| spellingShingle | Nikolaos P. Tzavellas Konstantinos I. Tsamis Andreas P. Katsenos Athena S. Davri Yannis V. Simos Ilias P. Nikas Stefanos Bellos Panagiotis Lekkas Foivos S. Kanellos Spyridon Konitsiotis Charalampos Labrakakis Patra Vezyraki Dimitrios Peschos Firing Alterations of Neurons in Alzheimer’s Disease: Are They Merely a Consequence of Pathogenesis or a Pivotal Component of Disease Progression? Cells Alzheimer’s disease neurophysiology pyramidal neurons interneurons LTP dendritic spine |
| title | Firing Alterations of Neurons in Alzheimer’s Disease: Are They Merely a Consequence of Pathogenesis or a Pivotal Component of Disease Progression? |
| title_full | Firing Alterations of Neurons in Alzheimer’s Disease: Are They Merely a Consequence of Pathogenesis or a Pivotal Component of Disease Progression? |
| title_fullStr | Firing Alterations of Neurons in Alzheimer’s Disease: Are They Merely a Consequence of Pathogenesis or a Pivotal Component of Disease Progression? |
| title_full_unstemmed | Firing Alterations of Neurons in Alzheimer’s Disease: Are They Merely a Consequence of Pathogenesis or a Pivotal Component of Disease Progression? |
| title_short | Firing Alterations of Neurons in Alzheimer’s Disease: Are They Merely a Consequence of Pathogenesis or a Pivotal Component of Disease Progression? |
| title_sort | firing alterations of neurons in alzheimer s disease are they merely a consequence of pathogenesis or a pivotal component of disease progression |
| topic | Alzheimer’s disease neurophysiology pyramidal neurons interneurons LTP dendritic spine |
| url | https://www.mdpi.com/2073-4409/13/5/434 |
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