Is there a molecular logic that sustains neuronal functional integrity and survival? Lipid signaling is necessary for neuroprotective neuronal transcriptional programs
Open accessAbstract
A challenge to civilization is the growing incidence in the loss of sight and cognition due to increased life expectancy. Therefore, we are confronted with a rise in the occurrence of photoreceptor- and neuronal-survival failure, as reflected mainly by age-related macular degeneration (AMD) and Alzheimer's disease (AD). Nervous system development is driven by neuronal apoptotic cell death, and thereafter, for the entire lifespan of an organism, neurons are postmitotic cells. In neurodegenerative diseases, apoptosis and other forms of cells death lead to selective neuronal loss. Although age is the main risk factor, not everyone develops these diseases during aging. Despite decades of important findings about neuronal cell death, the specific mechanisms that regulate neuronal survival remain incompletely understood.
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The failure of brain cells to survive ischemia-reperfusion damage may not be due to biology gone awry, but rather due to specific signals and mechanisms intended to be protective in the face of homeostasis disruptions that lead to neural circuits dysfunctions.
“The mechanistic cellular and molecular principles unraveled thus far should be instructive for stroke treatment translation because the failure of brain cells to survive ischemia-reperfusion damage may not be due to biology gone awry, but rather due to specific signals and mechanisms intended to be protective in the face of homeostasis disruptions that lead to neural circuits dysfunctions (Bazan,”
From Docosanoids and elovanoids from omega-3 fatty acids are pro-homeostatic modulators of inflammatory responses, cell damage and neuroprotection (2018) · cites this paper as Bazan, 2014
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References 29 · Cited by 15
Research works printed but not linked: 1
- [25]Calandria JM Asatryan A Balaszczuk V Knott E Jun BK Mukherjee PK Belayev L Bazan NG NPD1-mediated stereoselective regulation of BIRC3 expression through cREL is decisive for neural cell survival Cell Death Dis 2004 In press PMC4495360 25633199
- Authors
- Bazan, N. G.
- Affiliations
- Louisiana State University (US)
- Corresponding author
- Bazan, Nicolas G.
- ORCID
- Bazan, Nicolas G.
- Venue
- Molecular Neurobiology
- Published
- 2014-08
- Volume
- 50
- Issue
- 1
- Pages
- 1-5
- ISSN
- 0893-7648 (ISSN-L)
- 1559-1182
- PMC
- PMC4381928
- OpenAlex
- W2027429345
- Cited by
- 15
- References
- 29
- Citations by year
- 2025: 3 · 2022: 1 · 2019: 1 · 2018: 4 · 2017: 1 · 2016: 2 · 2015: 3
- FWCI
- 0.82
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Molecular Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Eye Institute (EY005121, R01EY005121)
- National Institute of General Medical Sciences (GM-103340, P30GM103340)
- National Institute of Neurological Disorders and Stroke (NS 046741, R01NS046741)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Sphingolipid Metabolism and Signaling
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- neuronal survival, neuroprotection, lipid signaling, apoptosis, age-related macular degeneration, Alzheimer's disease, photoreceptor loss, neurodegenerative diseases, neuronal cell death
- MeSH terms
- Aging, Cell Survival, Humans, Lipids, Neurons, Signal Transduction, Cell Death, Lipid Metabolism
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