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Hippocampal, Microglial, Morphological, and Amyloid Profiles Following Thiamine Pyrophosphate Treatment in 3xTg-AD
Nelly Jovana Pastén-Castrejón1,2, Humberto Martínez-Orozco2, Gloria Yareli Gutiérrez-Silerio1
1Laboratorio de Endocrinología y Nutrición, Facultad de Medicina, Centro de Investigación Biomédica Avanzada de la Universidad Autónoma de Querétaro, Santiago de Querétaro 76140, Mexico.
Abstract:
Alzheimer's disease (AD) is characterized by the accumulation of amyloid-β (Aβ) and chronic neuroinflammation, with microglia playing a central role in its pathogenesis. Alterations in microglial metabolism have been proposed to contribute to AD-related inflammatory responses and reduced Aβ clearance, suggesting that thiamine-dependent pathways may be relevant in this context. Thiamine pyrophosphate (TPP), the active form of vitamin B1, is essential for glucose metabolism and mitochondrial function; however, its association with microglial changes in AD remains unclear. In this study, 9-month-old female triple-transgenic AD (3xTg-AD) mice and non-transgenic controls (NoTg) received TPP (2.0 mg/mL) or saline as a vehicle for six weeks via osmotic pumps. Nesting, a hippocampus-dependent behavioral test, as well analyses of Aβ burden, microglial morphology, and the expression of genes related to metabolic and immune pathways were evaluated. Differences in nesting behavior between experimental groups were observed, but TPP treatment was not associated with an evident change in 3xTg-AD mice. In the subiculum and CA1 regions of the hippocampus of female 3xTg-AD mice exposed to TPP, a lower Aβ burden was observed, and morphological variations in microglia were detected in both groups (3xTg-AD and NoTg). Additionally, in the brain of the TPP-treated group, some changes in mRNA gene expression were recorded. Together, these findings describe hippocampal microglial and amyloid profiles following TPP treatment in 3xTg-AD mice and provide a basis for further investigation of thiamine-dependent pathways in AD-related neuroinflammatory contexts.
Insights
Thiamine pyrophosphate (TPP) treatment in Alzheimer's disease (AD) mice showed reduced amyloid-β burden in specific brain regions. Further research is needed to explore TPP's role in AD neuroinflammation.
Area of Science:
- Neuroscience
- Metabolic pathways
- Neuroinflammation
Background:
- Alzheimer's disease (AD) involves amyloid-β (Aβ) plaques and neuroinflammation, with microglia playing a key role.
- Altered microglial metabolism may impact AD pathogenesis, suggesting thiamine-dependent pathways are relevant.
- Thiamine pyrophosphate (TPP), the active form of vitamin B1, is crucial for metabolism, but its role in AD microglia is unknown.
Purpose of the Study:
- To investigate the effects of TPP treatment on microglial function, Aβ burden, and gene expression in a mouse model of AD.
- To assess behavioral changes and hippocampal pathology in response to TPP administration.
Main Methods:
- Female triple-transgenic AD (3xTg-AD) mice and non-transgenic (NoTg) controls received TPP or saline via osmotic pumps for six weeks.
- Evaluated nesting behavior, Aβ burden, microglial morphology, and gene expression in brain tissue.
- Hippocampal subiculum and CA1 regions were analyzed for Aβ deposition and microglial changes.
Main Results:
- TPP treatment led to reduced Aβ burden in the subiculum and CA1 of 3xTg-AD mouse hippocampi.
- Microglial morphology showed variations in both TPP-treated 3xTg-AD and NoTg mice.
- Some changes in brain mRNA gene expression were observed in the TPP-treated group.
- No significant changes in nesting behavior were noted in 3xTg-AD mice with TPP treatment.
Conclusions:
- TPP treatment influences hippocampal Aβ burden and microglial morphology in female 3xTg-AD mice.
- These findings highlight the potential of thiamine-dependent pathways in addressing AD-related neuroinflammation.
- Further investigation into TPP's therapeutic potential for Alzheimer's disease is warranted.
