Somatostatin, Olfaction, and Neurodegeneration

Saiz-Sánchez, Daniel; Úbeda-Bañón, Isabel; Flores‐Cuadrado, Alicia; González-Rodríguez, Melania; Villar‐Conde, Sandra; Astillero‐Lopez, Veronica; Martı́nez-Marcos, Alino

doi:10.3389/fnins.2020.00096

Cited by 28 publications

(26 citation statements)

References 59 publications

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“…Further studies showed that the decreased GABA neurotransmitter levels in the CSF were associated with age and AD (Bareggi et al, 1982;Zimmer et al, 1984;Grouselle et al, 1998;Li et al, 2016). SST expression was reduced by 50% in AD, which was related to the formation of Aβ oligomers (Saiz-Sanchez et al, 2020). SST might inhibit Aβ metabolism by upregulating neprilysin activity, with elevated neprilysin activity reducing the accumulation of both soluble and fibrillar Aβ in APP transgenic mice (Saito et al, 2005).…”

Section: Targeting Gaba Neurotransmittersmentioning

confidence: 99%

GABAergic Inhibitory Interneuron Deficits in Alzheimer’s Disease: Implications for Treatment

et al. 2020

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Alzheimer's disease (AD) is a neurodegenerative disorder characterized clinically by severe cognitive deficits and pathologically by amyloid plaques, neuronal loss, and neurofibrillary tangles. Abnormal amyloid β-protein (Aβ) deposition in the brain is often thought of as a major initiating factor in AD neuropathology. However, gammaaminobutyric acid (GABA) inhibitory interneurons are resistant to Aβ deposition, and Aβ decreases synaptic glutamatergic transmission to decrease neural network activity. Furthermore, there is now evidence suggesting that neural network activity is aberrantly increased in AD patients and animal models due to functional deficits in and decreased activity of GABA inhibitory interneurons, contributing to cognitive deficits. Here we describe the roles played by excitatory neurons and GABA inhibitory interneurons in Aβ-induced cognitive deficits and how altered GABA interneurons regulate AD neuropathology. We also comprehensively review recent studies on how GABA interneurons and GABA receptors can be exploited for therapeutic benefit. GABA interneurons are an emerging therapeutic target in AD, with further clinical trials urgently warranted.

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Section: Targeting Gaba Neurotransmittersmentioning

confidence: 99%

GABAergic Inhibitory Interneuron Deficits in Alzheimer’s Disease: Implications for Treatment

et al. 2020

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“…The AON, a key area of the olfactory system, shows accumulation of characteristic neuropathological markers such as hyperphosphorylated tau, α-synuclein and β-amyloid proteins at the earliest stages of AD in a Somatostatin (SST) expressing subpopulation of interneurons. In the limbic system, the same accumulation is evident in same subpopulation of interneurons [102]. However, SST is unequally involved in two predominant neurodegenerative disorders with a very strong involvement in AD pathology but quite weaker participation in PD.…”

Section: Drugsmentioning

confidence: 87%

“…However, SST is unequally involved in two predominant neurodegenerative disorders with a very strong involvement in AD pathology but quite weaker participation in PD. In early stages of AD, SST is reduced in olfactory areas whereas it is preserved in non-demented PD cases [102]. Further analysis of SST related olfactory deficiencies will pave the way of SST based therapeutic approaches.…”

Section: Drugsmentioning

confidence: 98%

Neurological and Neuropsychiatric Disorders in Relation to Olfactory Dysfunction

Bhatia‐Dey¹,

Heinbockel²

2020

Sino-Nasal and Olfactory System Disorders [Working Title]

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Olfaction is an underestimated sensory modality in terms of its predictive value as an indicator of disorders. It is a well-known phenomenon that a significant percentage of people afflicted with certain prevalent disorders causing degenerative neuropathology, progressive loss of memory and communication function, normal age-based decline of physiological functions, intellectual challenges, depressive and anxiety disorders as well as post-traumatic stress disorders, present with a range of olfactory deficits. Here, we review our understanding of these deficits and their relation to various clinical manifestations such as neurological and neuropsychiatric diseases and disorders. At the outset, we will briefly describe the olfactory pathway from olfactory sensory neurons in the nasal epithelium to the olfactory bulb and on to olfactory cortical and subcortical structures involved in olfaction such as the amygdala.

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“…Somatostatin (SST-14,28) is considered a universal endocrine molecule and a peptide hormone in the central nervous system (CNS), peripheral nervous system (PNS), and enteric nervous system (ENS) (1)(2)(3)(4)(5). It inhibits via different subtypes of SST receptors, and belongs to the superfamily of G protein-coupled receptors (GPCR) with 7-transmembrane domains.…”

Section: Introductionmentioning

confidence: 99%

“…It inhibits via different subtypes of SST receptors, and belongs to the superfamily of G protein-coupled receptors (GPCR) with 7-transmembrane domains. There are five SST receptors (SSTR1-5 and two isoforms SSTR2A, 2B), which are broadly expressed in the brain, spinal cord, dorsal root ganglion (DRGs), and ENS (1)(2)(3)(4)(5)(6). The gastrointestinal (GI) system is recognized to be the largest endocrine organ for digestion and absorption by exocrine, endocrine, paracrine, and autocrine secretory effects in animals during GI physiological and pathophysiological processes.…”

Section: Introductionmentioning

confidence: 99%

Versatile Functions of Somatostatin and Somatostatin Receptors in the Gastrointestinal System

Shamsi¹,

Chatoo²,

Xu³

et al. 2021

Front. Endocrinol.

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Somatostatin (SST) and somatostatin receptors (SSTRs) play an important role in the brain and gastrointestinal (GI) system. SST is produced in various organs and cells, and the inhibitory function of somatostatin-containing cells is involved in a range of physiological functions and pathological modifications. The GI system is the largest endocrine organ for digestion and absorption, SST-endocrine cells and neurons in the GI system are a critical effecter to maintain homeostasis via SSTRs 1-5 and co-receptors, while SST-SSTRs are involved in chemo-sensory, mucus, and hormone secretion, motility, inflammation response, itch, and pain via the autocrine, paracrine, endocrine, and exoendocrine pathways. It is also a power inhibitor for tumor cell proliferation, severe inflammation, and post-operation complications, and is a first-line anti-cancer drug in clinical practice. This mini review focuses on the current function of producing SST endocrine cells and local neurons SST-SSTRs in the GI system, discusses new development prognostic markers, phosphate-specific antibodies, and molecular imaging emerging in diagnostics and therapy, and summarizes the mechanism of the SST family in basic research and clinical practice. Understanding of endocrines and neuroendocrines in SST-SSTRs in GI will provide an insight into advanced medicine in basic and clinical research.

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Somatostatin, Olfaction, and Neurodegeneration

Cited by 28 publications

References 59 publications

GABAergic Inhibitory Interneuron Deficits in Alzheimer’s Disease: Implications for Treatment

GABAergic Inhibitory Interneuron Deficits in Alzheimer’s Disease: Implications for Treatment

Neurological and Neuropsychiatric Disorders in Relation to Olfactory Dysfunction

Versatile Functions of Somatostatin and Somatostatin Receptors in the Gastrointestinal System

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