Regulation of presynaptic homeostatic plasticity by glial signalling in Alzheimer's disease
Journal of Physiology, ISSN: 1469-7793
2024
- 4Captures
- 2Mentions
Metric Options: CountsSelecting the 1-year or 3-year option will change the metrics count to percentiles, illustrating how an article or review compares to other articles or reviews within the selected time period in the same journal. Selecting the 1-year option compares the metrics against other articles/reviews that were also published in the same calendar year. Selecting the 3-year option compares the metrics against other articles/reviews that were also published in the same calendar year plus the two years prior.
Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Captures4
- Readers4
- Mentions2
- News Mentions2
- News2
Most Recent News
Findings from Georgetown University Medical Center Broaden Understanding of Alzheimer Disease (Regulation of Presynaptic Homeostatic Plasticity By Glial Signalling In Alzheimer's Disease)
2025 JAN 14 (NewsRx) -- By a News Reporter-Staff News Editor at Pain & Central Nervous System Daily News -- Investigators discuss new findings in
Review Description
Alzheimer's disease (AD), the most common form of dementia among the elderly, affects numerous individuals worldwide. Despite advances in understanding the molecular underpinnings of AD pathology, effective treatments to prevent or cure the disease remain elusive. AD is characterized not only by pathological hallmarks such as amyloid plaques and neurofibrillary tangles but also by impairments in synaptic physiology, circuit activity and cognitive function. Synaptic homeostatic plasticity plays a vital role in maintaining the stability of synaptic and neural functions amid genetic and environmental disturbances. A key component of this regulation is presynaptic homeostatic potentiation, where increased presynaptic neurotransmitter release compensates for reduced postsynaptic glutamate receptor functionality, thereby stabilizing neuronal excitability. The role of presynaptic homeostatic plasticity in synapse stabilization in AD, however, remains unclear. Moreover, recent advances in transcriptomics have illuminated the complex roles of glial cells in regulating synaptic function in ageing brains and in the progression of neurodegenerative diseases. Yet, the impact of AD-related abnormalities in glial signalling on synaptic homeostatic plasticity has not been fully delineated. This review discusses recent findings on how glial dysregulation in AD affects presynaptic homeostatic plasticity. There is increasing evidence that disrupted glial signalling, particularly through aberrant histone acetylation and transcriptomic changes in glia, compromises this plasticity in AD. Notably, the sphingosine signalling pathway has been identified as being protective in stabilizing synaptic physiology through epigenetic and homeostatic mechanisms, presenting potential therapeutic targets for treating neurodegenerative disorders. (Figure presented.).
Bibliographic Details
Provide Feedback
Have ideas for a new metric? Would you like to see something else here?Let us know