Alzheimer’s Disease as a Result of Stimulus Reduction in a GABA-A-Deficient Brain: A Neurocomputational Model
Several research studies point to the fact that sensory and cognitive reductions like cataracts, deafness, macular degeneration, or even lack of activity after job retirement, precede the onset of Alzheimer’s disease. To simulate Alzheimer’s disease earlier stages, which manifest in sensory cortices...
Saved in:
| Main Authors: | , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
2020-01-01
|
| Series: | Neural Plasticity |
| Online Access: | http://dx.doi.org/10.1155/2020/8895369 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1832563422266392576 |
|---|---|
| author | Mariana Antonia Aguiar-Furucho Francisco Javier Ropero Peláez |
| author_facet | Mariana Antonia Aguiar-Furucho Francisco Javier Ropero Peláez |
| author_sort | Mariana Antonia Aguiar-Furucho |
| collection | DOAJ |
| description | Several research studies point to the fact that sensory and cognitive reductions like cataracts, deafness, macular degeneration, or even lack of activity after job retirement, precede the onset of Alzheimer’s disease. To simulate Alzheimer’s disease earlier stages, which manifest in sensory cortices, we used a computational model of the koniocortex that is the first cortical stage processing sensory information. The architecture and physiology of the modeled koniocortex resemble those of its cerebral counterpart being capable of continuous learning. This model allows one to analyze the initial phases of Alzheimer’s disease by “aging” the artificial koniocortex through synaptic pruning, by the modification of acetylcholine and GABA-A signaling, and by reducing sensory stimuli, among other processes. The computational model shows that during aging, a GABA-A deficit followed by a reduction in sensory stimuli leads to a dysregulation of neural excitability, which in the biological brain is associated with hypermetabolism, one of the earliest symptoms of Alzheimer’s disease. |
| format | Article |
| id | doaj-art-3fd4f633fd1a4d298873193cc3214cf1 |
| institution | Kabale University |
| issn | 2090-5904 1687-5443 |
| language | English |
| publishDate | 2020-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Neural Plasticity |
| spelling | doaj-art-3fd4f633fd1a4d298873193cc3214cf12025-02-03T01:20:09ZengWileyNeural Plasticity2090-59041687-54432020-01-01202010.1155/2020/88953698895369Alzheimer’s Disease as a Result of Stimulus Reduction in a GABA-A-Deficient Brain: A Neurocomputational ModelMariana Antonia Aguiar-Furucho0Francisco Javier Ropero Peláez1Engineering, Neuroscience and Bio-Inspired Systems Study Group (GENeSis), Department of Electrotechnics (DAELT), Universidade Tecnológica Federal do Paraná (UTFPR), Paraná 80230-901, BrazilCenter for Neuroscience and Behavior, Institute of Psychology, University of São Paulo, São Paulo, BrazilSeveral research studies point to the fact that sensory and cognitive reductions like cataracts, deafness, macular degeneration, or even lack of activity after job retirement, precede the onset of Alzheimer’s disease. To simulate Alzheimer’s disease earlier stages, which manifest in sensory cortices, we used a computational model of the koniocortex that is the first cortical stage processing sensory information. The architecture and physiology of the modeled koniocortex resemble those of its cerebral counterpart being capable of continuous learning. This model allows one to analyze the initial phases of Alzheimer’s disease by “aging” the artificial koniocortex through synaptic pruning, by the modification of acetylcholine and GABA-A signaling, and by reducing sensory stimuli, among other processes. The computational model shows that during aging, a GABA-A deficit followed by a reduction in sensory stimuli leads to a dysregulation of neural excitability, which in the biological brain is associated with hypermetabolism, one of the earliest symptoms of Alzheimer’s disease.http://dx.doi.org/10.1155/2020/8895369 |
| spellingShingle | Mariana Antonia Aguiar-Furucho Francisco Javier Ropero Peláez Alzheimer’s Disease as a Result of Stimulus Reduction in a GABA-A-Deficient Brain: A Neurocomputational Model Neural Plasticity |
| title | Alzheimer’s Disease as a Result of Stimulus Reduction in a GABA-A-Deficient Brain: A Neurocomputational Model |
| title_full | Alzheimer’s Disease as a Result of Stimulus Reduction in a GABA-A-Deficient Brain: A Neurocomputational Model |
| title_fullStr | Alzheimer’s Disease as a Result of Stimulus Reduction in a GABA-A-Deficient Brain: A Neurocomputational Model |
| title_full_unstemmed | Alzheimer’s Disease as a Result of Stimulus Reduction in a GABA-A-Deficient Brain: A Neurocomputational Model |
| title_short | Alzheimer’s Disease as a Result of Stimulus Reduction in a GABA-A-Deficient Brain: A Neurocomputational Model |
| title_sort | alzheimer s disease as a result of stimulus reduction in a gaba a deficient brain a neurocomputational model |
| url | http://dx.doi.org/10.1155/2020/8895369 |
| work_keys_str_mv | AT marianaantoniaaguiarfurucho alzheimersdiseaseasaresultofstimulusreductioninagabaadeficientbrainaneurocomputationalmodel AT franciscojavierroperopelaez alzheimersdiseaseasaresultofstimulusreductioninagabaadeficientbrainaneurocomputationalmodel |