2021
DOI: 10.3389/fnins.2020.618395
|View full text |Cite
|
Sign up to set email alerts
|

Abstract: Over the past decades, the human life span has dramatically increased, and therefore, a steady increase in diseases associated with age (such as Alzheimer’s disease and Parkinson’s disease) is expected. In these neurodegenerative diseases, there is a cognitive decline and memory loss, which accompany increased systemic inflammation, the inflamm-aging, and the insulin resistance. Despite numerous studies of age-related pathologies, data on the contribution of brain insulin resistance and innate immunity compone… Show more

Help me understand this report
View preprint versions

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
2
1

Citation Types

1
17
0
4

Year Published

2021
2021
2024
2024

Publication Types

Select...
6
1

Relationship

1
6

Authors

Journals

citations
Cited by 27 publications
(22 citation statements)
references
References 154 publications
(164 reference statements)
1
17
0
4
Order By: Relevance
“…Therefore, it can be assumed that the absence of a normal background immune response in NLRP3 KO mice in the form of an IL-1β-mediated signaling cascade disrupts insulin-dependent plasticity and leads to effects opposite to those found in WT animals. The observed Aβ effect on insulin-mediated dynamics of the fEPSP amplitudes also correlates with the data described in the literature and fits into the theory of insulin resistance in neurodegenerative diseases such as Alzheimer’s disease [ 12 , 19 , 56 , 57 ]. As noted above, insulin, via insulin receptors on the neuron surface, induces clathrin-mediated intralization of AMPA receptors, which leads to a long-term decrease in amplitude [ 58 ].…”
Section: Discussionsupporting
confidence: 87%
See 3 more Smart Citations
“…Therefore, it can be assumed that the absence of a normal background immune response in NLRP3 KO mice in the form of an IL-1β-mediated signaling cascade disrupts insulin-dependent plasticity and leads to effects opposite to those found in WT animals. The observed Aβ effect on insulin-mediated dynamics of the fEPSP amplitudes also correlates with the data described in the literature and fits into the theory of insulin resistance in neurodegenerative diseases such as Alzheimer’s disease [ 12 , 19 , 56 , 57 ]. As noted above, insulin, via insulin receptors on the neuron surface, induces clathrin-mediated intralization of AMPA receptors, which leads to a long-term decrease in amplitude [ 58 ].…”
Section: Discussionsupporting
confidence: 87%
“…This is important for long-term memory consolidation. Similar to IL-1β action, as described by Goshen and colleagues, physiological levels of NLRP3 promote memory formation [ 12 ], and NLRP3 inflammasomes are required for insulin-dependent glucose transport in the brain. At the same time, NLRP3 knockout ameliorates insulin resistance during the development of amyloid-induced neurodegeneration.…”
Section: Discussionmentioning
confidence: 93%
See 2 more Smart Citations
“…These events lead to significant changes in neuronal metabolism like elevated glucose utilization and conversion to lactate, facilitation of mitochondrial oxidative phosphorylation (OXPHOS) [ 81 ]. Thus, it is not surprising that aberrant insulin signaling and brain glucose hypometabolism are considered as components of the pathogenesis of Alzheimer’s disease and progression of physiological aging: these metabolic phenomena trigger a cascade of pathological events, namely mitochondrial dysfunction, oxidative stress, excitotoxicity, apoptosis, and activation of pro-inflammatory cytokines [ 81 , 82 , 83 , 84 ] ( Figure 1 ). Recently, systemic insulin resistance and development of diabetes mellitus in ageing mice (P350) that underwent ELS in the form of maternal separation at the neonatal period was clearly demonstrated [ 85 ], but whether these data might be extrapolated on the cerebral mechanisms of insulin signaling remains unclear.…”
Section: Developmental Aspects Of Brain Metabolism and Effects Of Elsmentioning
confidence: 99%