Cited by 32Olfactory and Sensory Function StudiesAlzheimer's disease research and treatmentsParkinson's Disease Mechanisms and Treatments

Somatostatin, Olfaction, and Neurodegeneration

Open access
Saiz-Sanchez, Daniel, Ubeda-Bañon, Isabel, Flores-Cuadrado, Alicia, Gonzalez-Rodriguez, Melania, Villar-Conde, Sandra, Astillero-Lopez, Veronica, Martinez-Marcos, Alino·2020·Frontiers in Neuroscience

Abstract

Alzheimer's and Parkinson's diseases are the most prevalent neurodegenerative disorders in aging. Hyposmia has been described as an early symptom that can precede cognitive and motor deficits by decades. Certain regions within the olfactory system, such as the anterior olfactory nucleus, display the neuropathological markers tau and amyloid-β or α-synuclein from the earliest stages of disease progression in a preferential manner. Specific neuronal subpopulations, namely those expressing somatostatin (SST), are preferentially affected throughout the olfactory and limbic systems. SST is a neuropeptide present in a subpopulation of GABAergic interneurons throughout the brain and its main function is to inhibit principal neurons and/or other interneurons. It has been reported that SST expression is reduced by 50% in Alzheimer's disease and that it is related to the formation of Aβ oligomers. The mechanisms underlying the preferential vulnerability of SST-expressing neurons in Alzheimer's disease (and, to a minor extent, in Parkinson's disease) are not known but analysis of the available data could shed light on their etiology. This short review aims to update the knowledge of functional features of somatostatin within the olfactory system and its role in olfactory deficits during neurodegeneration.

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Crossref · 10.3389/fnins.2020.00096

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  • The expression of SST and KCNIP1 is reduced in the brains of individuals with AD, and downregulation of these two genes has been implicated in mediating the formation of Aβ oligomers.

    “The expression of SST (61) and KCNIP1 (62) is reduced in the brains of individuals with AD, and downregulation of these two genes has been implicated in mediating the formation of Aβ oligomers.”

    From Modeling late-onset Alzheimer’s disease neuropathology via direct neuronal reprogramming (2024) · cites this paper as [61]

    The 'Somatostatin and Alzheimer’s Disease' section reports reduced SST in AD and says SST can encourage Aβ oligomer formation. It does not say that SST downregulation mediates oligomer formation. KCNIP1 is attached to a different citation in the citing sentence, so it is not assessed against this source. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

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Research works printed but not linked: 1

  1. Mai J. Majtanik M. Paxinos G. (2015). Atlas of the Human Brain. Cambridge, MA: Academic Press.

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Authors
Saiz-Sanchez, D., Ubeda-Bañon, I., Flores-Cuadrado, A., Gonzalez-Rodriguez, M., Villar-Conde, S., Astillero-Lopez, V., & Martinez-Marcos, A.
Venue
Frontiers in Neuroscience
Published
2020-02-19
Volume
14
Pages
96-96
ISSN
1662-453X (ISSN-L)
OpenAlex
W3008187938
Cited by
32
References
60
Citations by year
2026: 4 · 2025: 2 · 2024: 8 · 2023: 9 · 2022: 1 · 2021: 4 · 2020: 4
FWCI
0.59
Type
journal article
Language
en
Open access
Locations
  • Frontiers in Neuroscience (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • RUIdeRA - Institutional University Repository (University of Castilla-La Mancha) (submittedVersion, other-oa)
Funders
  • Junta de Comunidades de Castilla-La Mancha
  • Ministerio de Economía, Industria y Competitividad, Gobierno de España
Topics
  • Life Sciences › Neuroscience › Sensory Systems › Olfactory and Sensory Function Studies
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
Keywords
somatostatin, olfaction, hyposmia, neurodegeneration, Alzheimer's disease, Parkinson's disease, olfactory system, anterior olfactory nucleus, GABAergic interneurons, tau protein, amyloid-beta, alpha-synuclein, amyloid-beta oligomers, neuronal vulnerability

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