ArticleASN neuro
Altered Brain Expression of Insulin and Insulin-Like Growth Factors in Frontotemporal Lobar Degeneration: Another Degenerative Disease Linked to Dysregulation of Insulin Metabolic Pathways.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Insulin-like growth factor 1 associated research in Alzheimer's disease: an exploratory trends analysis.Frontiers in neurologyPooled it
- Uncovering pathophysiological changes in frontotemporal dementia using serum lipids.Scientific reports · 2020Trial
- Article
- Biological pathways related to mirna-125a-5p in behavioral variant of frontotemporal dementia.Molecular biology reports · 2026Article
- Exploring the PLD1-tau interaction in Frontotemporal Dementia.bioRxiv : the preprint server for biology · 2026Article
- Alterations to metabolic hormones in amyotrophic lateral sclerosis and frontotemporal dementia postmortem human tissue.Journal of neuropathology and experimental neurology · 2024Article
- PCDHA9 as a candidate gene for amyotrophic lateral sclerosis.Nature communications · 2024Article
- Agent Orange Herbicidal Toxin-Initiation of Alzheimer-Type Neurodegeneration.Journal of Alzheimer's disease : JAD · 2024Article
- Dysregulated mTOR networks in experimental sporadic Alzheimer's disease.Frontiers in cellular neuroscience · 2024Article
- Conquering Insulin Network Dysfunctions in Alzheimer's Disease: Where Are We Today?Journal of Alzheimer's disease : JAD · 2024Review
- The neurobiology of insulin-like growth factor I: From neuroprotection to modulation of brain states.Molecular psychiatry · 2023Review
- Repositioning of Anti-Diabetic Drugs against Dementia: Insight from Molecular Perspectives to Clinical Trials.International journal of molecular sciences · 2023Review
- Molecular mechanisms underlying hyperglycemia associated cognitive decline.IBRO neuroscience reports · 2023Review
- IGF2 in memory, neurodevelopmental disorders, and neurodegenerative diseases.Trends in neurosciences · 2023Review
- Agent Orange Causes Metabolic Dysfunction and Molecular Pathology Reminiscent of Alzheimer's Disease.Journal of Alzheimer's disease reports · 2023Article
- Conserved gene signatures shared amongFrontiers in molecular biosciences · 2023Article
- Multiple pathways of lipid dysregulation in amyotrophic lateral sclerosis.Brain communications · 2023Article
- Exosomal MicroRNAs in Military Personnel with Mild Traumatic Brain Injury: Preliminary Results from the Chronic Effects of Neurotrauma Consortium Biomarker Discovery Project.Journal of neurotrauma · 2020Observational
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4 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundFrontotemporal lobar degeneration (FTLD) is the third most common dementing neurodegenerative disease with nearly 80% having no known etiology.
objectiveGrowing 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.
methodsPostmortem 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.
resultsFTLD 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.
conclusionsAberrantly 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.
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