Prenatal stress aggravates age-dependent cognitive decline, insulin signaling dysfunction, and the pro-inflammatory response in the APPNL-F/NL-F mouse model of Alzheimer's disease

Trojan, Ewa; Curzytek, Katarzyna; Cieślik, Paulina; Wierońska, Joanna M.; Gräff, Johannes; Lasoń, Władysław; Saito, Takashi; Saido, Takaomi C.; Basta‐Kaim, Agnieszka

doi:10.1016/j.nbd.2023.106219

Cited by 2 publications

(1 citation statement)

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“…In mice with APP mutations, cortical IGF1R expression is reported to be down-regulated [43], and short-term peripheral administration of IGF-I has no effect on CSF or plasma Aβ concentrations [44]. Prenatal stress aggravates the APP phenotype [45]. When crossed with mice deficient for IRS-2, Aβ accumulation is delayed, and premature mortality is reversed in female mice [46].…”

Section: Alzheimer's Disease (Ad)mentioning

confidence: 99%

Role of the Insulin-like Growth Factor System in Neurodegenerative Disease

Lewitt,

Boyd

2024

IJMS

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The insulin-like growth factor (IGF) system has paracrine and endocrine roles in the central nervous system. There is evidence that IGF signalling pathways have roles in the pathophysiology of neurodegenerative disease. This review focusses on Alzheimer’s disease and Parkinson’s disease, the two most common neurodegenerative disorders that are increasing in prevalence globally in relation to the aging population and the increasing prevalence of obesity and type 2 diabetes. Rodent models used in the study of the molecular pathways involved in neurodegeneration are described. However, currently, no animal model fully replicates these diseases. Mice with triple mutations in APP, PSEN and MAPT show promise as models for the testing of novel Alzheimer’s therapies. While a causal relationship is not proven, the fact that age, obesity and T2D are risk factors in both strengthens the case for the involvement of the IGF system in these disorders. The IGF system is an attractive target for new approaches to management; however, there are gaps in our understanding that first need to be addressed. These include a focus beyond IGF-I on other members of the IGF system, including IGF-II, IGF-binding proteins and the type 2 IGF receptor.

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