125I-insulin binding is decreased in olfactory bulbs of aged rats

Tchilian, Elma; Zhelezarov, I.E.; Petkov, V.; Hadjiivanova, Ch.

doi:10.1016/0143-4179(90)90035-w

Cited by 22 publications

(15 citation statements)

References 19 publications

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“…The high density of IRs in the brain of postmortem human's fetus and their decrease as a function of age has also been reported [79]. Although a similar age-dependent decrease in IR density was mentioned by other researchers [64,[80][81][82], Tchilian et al reported that the decrease in receptor density is confined to the olfactory bulb, while other regions like the frontal cortex, hippocampus, and hypothalamus did not show any significant agedependent changes in IR density [83]. A developmental change in properties of IRs has been also reported.…”

Section: Developmental Pattern Of Ir Distribution Throughout the Brainmentioning

confidence: 78%

Insulin in the Brain: Sources, Localization and Functions

et al. 2012

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Historically, insulin is best known for its role in peripheral glucose homeostasis, and insulin signaling in the brain has received less attention. Insulin-independent brain glucose uptake has been the main reason for considering the brain as an insulin-insensitive organ. However, recent findings showing a high concentration of insulin in brain extracts, and expression of insulin receptors (IRs) in central nervous system tissues have gathered considerable attention over the sources, localization, and functions of insulin in the brain. This review summarizes the current status of knowledge of the peripheral and central sources of insulin in the brain, site-specific expression of IRs, and also neurophysiological functions of insulin including the regulation of food intake, weight control, reproduction, and cognition and memory formation. This review also considers the neuromodulatory and neurotrophic effects of insulin, resulting in proliferation, differentiation, and neurite outgrowth, introducing insulin as an attractive tool for neuroprotection against apoptosis, oxidative stress, beta amyloid toxicity, and brain ischemia.

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Section: Developmental Pattern Of Ir Distribution Throughout the Brainmentioning

confidence: 78%

Insulin in the Brain: Sources, Localization and Functions

et al. 2012

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“…If the change in the cell turnover of the OB represents the primary change, changes in cell turnover may reflect changes in the availability of growth factors. It has been reported that the expression of IGF-1 decreases with age (Ferrari et al, 2003 ; Chaker et al, 2015 ) and that insulin binding decreases in the OB with age, probably because of the decrease in the insulin receptor number in the OB (Tchilian et al, 1990 ). The accumulation of oxidative stress and the resulting cell aging may also cause age-related changes in the OB (Vaishnav et al, 2007 ; Romero-Grimaldi et al, 2008 ).…”

Section: Age-related Changes In the Structure And Cell Dynamics Of Thmentioning

confidence: 99%

Age-Related Olfactory Dysfunction: Epidemiology, Pathophysiology, and Clinical Management

Kondo

Kikuta

Ueha

et al. 2020

Front. Aging Neurosci.

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Like other sensory systems, olfactory function deteriorates with age. Epidemiological studies have revealed that the incidence of olfactory dysfunction increases at the age of 60 and older and males are more affected than females. Moreover, smoking, heavy alcohol use, sinonasal diseases, and Down's syndrome are associated with an increased incidence of olfactory dysfunction. Although the pathophysiology of olfactory dysfunction in humans remains largely unknown, studies in laboratory animals have demonstrated that both the peripheral and central olfactory nervous systems are affected by aging. Aged olfactory neuroepithelium in the nasal cavity shows the loss of mature olfactory neurons, replacement of olfactory neuroepithelium by respiratory epithelium, and a decrease in basal cell proliferation both in the normal state and after injury. In the central olfactory pathway, a decrease in the turnover of interneurons in the olfactory bulb (OB) and reduced activity in the olfactory cortex under olfactory stimulation is observed. Recently, the association between olfactory impairment and neurodegenerative diseases, such as Alzheimer's disease (AD) and Parkinson's disease (PD), has gained attention. Evidence-based pharmacotherapy to suppress or improve age-related olfactory dysfunction has not yet been established, but preliminary results suggest that olfactory training using odorants may be useful to improve some aspects of age-related olfactory impairment.

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“…Insulin and IGF-1 interact in regulation of glucose disposal [34] and IGF-1 mimic insulin signalling in the brain [35], suggesting a partial overlapping. Several studies have shown the highest IR density in olfactory bulb, hippocampal formation, hypothalamus and cerebral cortex [36]. In post-mortem studies in adult humans, Adem et al .…”

Section: Insulin Igf-1 In the Brainmentioning

confidence: 99%

Possible implications of insulin resistance and glucose metabolism in Alzheimer’s disease pathogenesis

Bosco

Fava²,

Plastino

et al. 2011

Journal of Cellular and Molecular Medicine

243

164

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Type 2 diabetes mellitus (DM) appears to be a significant risk factor for Alzheimer disease (AD). Insulin and insulin-like growth factor-1 (IGF-1) also have intense effects in the central nervous system (CNS), regulating key processes such as neuronal survival and longevity, as well as learning and memory. Hyperglycaemia induces increased peripheral utilization of insulin, resulting in reduced insulin transport into the brain. Whereas the density of brain insulin receptor decreases during age, IGF-1 receptor increases, suggesting that specific insulin-mediated signals is involved in aging and possibly in cognitive decline. Molecular mechanisms that protect CNS neurons against β-amyloid-derived-diffusible ligands (ADDL), responsible for synaptic deterioration underlying AD memory failure, have been identified. The protection mechanism does not involve simple competition between ADDLs and insulin, but rather it is signalling dependent down-regulation of ADDL-binding sites. Defective insulin signalling make neurons energy deficient and vulnerable to oxidizing or other metabolic insults and impairs synaptic plasticity. In fact, destruction of mitochondria, by oxidation of a dynamic-like transporter protein, may cause synapse loss in AD. Moreover, interaction between Aβ and τ proteins could be cause of neuronal loss. Hyperinsulinaemia as well as complete lack of insulin result in increased τ phosphorylation, leading to an imbalance of insulin-regulated τ kinases and phosphatates. However, amyloid peptides accumulation is currently seen as a key step in the pathogenesis of AD. Inflammation interacts with processing and deposit of β-amyloid. Chronic hyperinsulinemia may exacerbate inflammatory responses and increase markers of oxidative stress. In addition, insulin appears to act as ‘neuromodulator’, influencing release and reuptake of neurotransmitters, and improving learning and memory. Thus, experimental and clinical evidence show that insulin action influences cerebral functions. In this paper, we reviewed several mechanisms by which insulin may affect pathophysiology in AD.

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125I-insulin binding is decreased in olfactory bulbs of aged rats

Cited by 22 publications

References 19 publications

Insulin in the Brain: Sources, Localization and Functions

Insulin in the Brain: Sources, Localization and Functions

Age-Related Olfactory Dysfunction: Epidemiology, Pathophysiology, and Clinical Management

Possible implications of insulin resistance and glucose metabolism in Alzheimer’s disease pathogenesis

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