Altered Brain Expression of Insulin and Insulin-Like Growth Factors in Frontotemporal Lobar Degeneration: Another Degenerative Disease Linked to Dysregulation of Insulin Metabolic Pathways.


Journal

ASN neuro
ISSN: 1759-0914
Titre abrégé: ASN Neuro
Pays: United States
ID NLM: 101507115

Informations de publication

Date de publication:
Historique:
entrez: 14 5 2019
pubmed: 14 5 2019
medline: 14 5 2020
Statut: ppublish

Résumé

Frontotemporal lobar degeneration (FTLD) is the third most common dementing neurodegenerative disease with nearly 80% having no known etiology. Growing evidence that neurodegeneration can be linked to dysregulated metabolism prompted us to measure a panel of trophic factors, receptors, and molecules that modulate brain metabolic function in FTLD. Postmortem frontal (Brodmann's area [BA]8/9 and BA24) and temporal (BA38) lobe homogenates were used to measure immunoreactivity to Tau, phosphorylated tau (pTau), ubiquitin, 4-hydroxynonenal (HNE), transforming growth factor-beta 1 (TGF-β1) and its receptor (TGF-β1R), brain-derived neurotrophic factor (BDNF), nerve growth factor, neurotrophin-3, neurotrophin-4, tropomyosin receptor kinase, and insulin and insulin-like growth factor-1 (IGF-1) and insulin-like growth factor-2 (IGF-2) and their receptors by direct-binding enzyme-linked immunosorbent assay. FTLD brains had significantly elevated pTau, ubiquitin, TGF-β1, and HNE immunoreactivity relative to control. In addition, BDNF and neurotrophin-4 were respectively reduced in BA8/9 and BA38, while neurotrophin-3 and nerve growth factor were upregulated in BA38, and tropomyosin receptor kinase was elevated in BA24. Lastly, insulin and insulin receptor expressions were elevated in the frontal lobe, IGF-1 was increased in BA24, IGF-1R was upregulated in all three brain regions, and IGF-2 receptor was reduced in BA24 and BA38. Aberrantly increased levels of pTau, ubiquitin, HNE, and TGF-β1, marking neurodegeneration, oxidative stress, and neuroinflammation, overlap with altered expression of insulin/IGF signaling ligand and receptors in frontal and temporal lobe regions targeted by FTLD. Dysregulation of insulin-IGF signaling networks could account for brain hypometabolism and several characteristic neuropathologic features that characterize FTLD but overlap with Alzheimer's disease, Parkinson's disease, and Dementia with Lewy Body Disease.

Sections du résumé

BACKGROUND
Frontotemporal lobar degeneration (FTLD) is the third most common dementing neurodegenerative disease with nearly 80% having no known etiology.
OBJECTIVE
Growing evidence that neurodegeneration can be linked to dysregulated metabolism prompted us to measure a panel of trophic factors, receptors, and molecules that modulate brain metabolic function in FTLD.
METHODS
Postmortem frontal (Brodmann's area [BA]8/9 and BA24) and temporal (BA38) lobe homogenates were used to measure immunoreactivity to Tau, phosphorylated tau (pTau), ubiquitin, 4-hydroxynonenal (HNE), transforming growth factor-beta 1 (TGF-β1) and its receptor (TGF-β1R), brain-derived neurotrophic factor (BDNF), nerve growth factor, neurotrophin-3, neurotrophin-4, tropomyosin receptor kinase, and insulin and insulin-like growth factor-1 (IGF-1) and insulin-like growth factor-2 (IGF-2) and their receptors by direct-binding enzyme-linked immunosorbent assay.
RESULTS
FTLD brains had significantly elevated pTau, ubiquitin, TGF-β1, and HNE immunoreactivity relative to control. In addition, BDNF and neurotrophin-4 were respectively reduced in BA8/9 and BA38, while neurotrophin-3 and nerve growth factor were upregulated in BA38, and tropomyosin receptor kinase was elevated in BA24. Lastly, insulin and insulin receptor expressions were elevated in the frontal lobe, IGF-1 was increased in BA24, IGF-1R was upregulated in all three brain regions, and IGF-2 receptor was reduced in BA24 and BA38.
CONCLUSIONS
Aberrantly increased levels of pTau, ubiquitin, HNE, and TGF-β1, marking neurodegeneration, oxidative stress, and neuroinflammation, overlap with altered expression of insulin/IGF signaling ligand and receptors in frontal and temporal lobe regions targeted by FTLD. Dysregulation of insulin-IGF signaling networks could account for brain hypometabolism and several characteristic neuropathologic features that characterize FTLD but overlap with Alzheimer's disease, Parkinson's disease, and Dementia with Lewy Body Disease.

Identifiants

pubmed: 31081340
doi: 10.1177/1759091419839515
pmc: PMC6535914
doi:

Substances chimiques

Insulin 0
Somatomedins 0

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

1759091419839515

Subventions

Organisme : NIAAA NIH HHS
ID : R01 AA012908
Pays : United States
Organisme : NIAAA NIH HHS
ID : R37 AA011431
Pays : United States

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Auteurs

Connie J Liou (CJ)

1 Warren Alpert Medical School of Brown University, Providence, RI, USA.

Ming Tong (M)

1 Warren Alpert Medical School of Brown University, Providence, RI, USA.
2 Division of Neuropathology, Departments of Pathology, Medicine, Neurology, and Neurosurgery, Rhode Island Hospital, Providence, RI, USA.
3 Department of Pathology and Laboratory Medicine, the Providence VA Medical Center, Providence, RI, USA.

Jean P Vonsattel (JP)

4 New York Brain Bank, Taub Institute, Columbia University, New York, NY, USA.

Suzanne M de la Monte (SM)

1 Warren Alpert Medical School of Brown University, Providence, RI, USA.
2 Division of Neuropathology, Departments of Pathology, Medicine, Neurology, and Neurosurgery, Rhode Island Hospital, Providence, RI, USA.
3 Department of Pathology and Laboratory Medicine, the Providence VA Medical Center, Providence, RI, USA.

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