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Localization of Thioredoxin-Interacting Protein in Aging and Alzheimer's Disease Brains

Localization of Thioredoxin-Interacting Protein in Aging and Alzheimer's Disease Brains

Haruka Tsubaki ¹, Anarmaa Mendsaikhan ^1,2, Undral Buyandelger ¹, Ikuo Tooyama ¹, Douglas G Walker ^1,3

Haruka Tsubaki ¹, Anarmaa Mendsaikhan ^1,2, Undral Buyandelger ¹

¹Molecular Neuroscience Research Center, Shiga University of Medical Science, Otsu 520-2192, Japan; ds111857@g.shiga-med.ac.jp (H.T.); anarmaa.mendsaikhan@emory.edu (A.M.); undraa.b12@gmail.com (U.B.); kincan@belle.shiga-med.ac.jp (I.T.).
²Department of Pharmacology, Emory University School of Medicine, Atlanta, GA 30322, USA.
³Neurodegenerative Disease Research Center, Arizona State University, Tempe, AZ 85281, USA.

⁰Molecular Neuroscience Research Center, Shiga University of Medical Science, Otsu 520-2192, Japan; ds111857@g.shiga-med.ac.jp (H.T.); anarmaa.mendsaikhan@emory.edu (A.M.); undraa.b12@gmail.com (U.B.); kincan@belle.shiga-med.ac.jp (I.T.).

Neurosci +

|

November 1, 2024

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View abstract on PubMed

Summary

This summary is machine-generated.

Thioredoxin-Interacting Protein (TXNIP) expression changes in Alzheimer

Area Of Science

Neuroscience
Molecular Biology
Pathology

Background

Thioredoxin-Interacting Protein (TXNIP) plays a pathogenic role in diseases linked to diabetes and hyperglycemia.
TXNIP sequesters thioredoxins, leading to increased oxidative stress.
Understanding TXNIP's role in neurodegenerative diseases like Alzheimer's is crucial.

Purpose Of The Study

To investigate the cellular expression patterns of TXNIP in human aged and Alzheimer's disease (AD) brains.
To determine if TXNIP expression correlates with pathological structures in AD.
To analyze TXNIP levels in neuronal and glial cells in relation to AD progression.

Main Methods

Utilized fixed tissue sections and protein extracts from temporal cortex of AD and aged control brains.
Employed light and fluorescent immunohistochemistry with the JY2 monoclonal antibody to detect TXNIP.
Quantified TXNIP protein levels using immunoblots.

Main Results

TXNIP immunoreactivity was observed in specific neuronal populations, particularly in non-AD brains.
AD brains showed reduced neuronal TXNIP but increased TXNIP-positive microglia associated with plaques.
Immunoblot analysis revealed no significant change in overall TXNIP protein levels in AD samples.

Conclusions

Cellular expression patterns of TXNIP are altered in human brains with Alzheimer's disease progression.
TXNIP localization shifts from neurons to plaque-associated microglia in AD.
These findings highlight a potential role for TXNIP dysregulation in AD pathogenesis.

Keywords:

amyloid plaque human tissue immunohistochemistry inflammasome inflammation microglia neuropathology oxidative stress

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