Progesterone restores mitochondrial bioenergetic function in streptozotocin- and amyloid-β-challenged HT-22 hippocampal cells: An in vitro model of Alzheimer's disease
- 1Department of Radiation Oncology, , Atlanta, GA,
- 2Department of Emergency Medicine, , Atlanta, GA,
- 3, Atlanta, GA,
Abstract
Background Mitochondrial dysfunction contributes to Alzheimer's disease (AD) by promoting bioenergetic failure and neuronal loss. Objective We investigated whether progesterone (P4) protects against mitochondrial impairment in two in vitro AD models. Methods Mouse hippocampal HT-22 cells were exposed to amyloid-β (Aβ) or streptozotocin (STZ) and treated with P4. Mitochondrial respiration was assessed using Seahorse extracellular flux analysis. Results Both Aβ and STZ significantly reduced basal and maximal respiration, spare respiratory capacity, and ATP-linked respiration (ATP production rate), while increasing proton leak and cell death. P4 treatment restored mitochondrial respiratory parameters and improved cell viability. Conclusions These findings suggest progesterone preserves mitochondrial bioenergetic function under AD-related stress conditions.
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BibTeX
@article{yousuf2026progesterone,
title = {{Progesterone restores mitochondrial bioenergetic function in streptozotocin- and amyloid-β-challenged HT-22 hippocampal cells: An in vitro model of Alzheimer's disease}},
author = {Seema Yousuf and Fahim Atif and Donald G. Stein},
journal = {Journal of Alzheimer's Disease Reports},
year = {2026},
month = oct,
doi = {10.1177/25424823261498338},
url = {https://doi.org/10.1177/25424823261498338},
note = {CC BY},
}
RIS
TY - JOUR
TI - Progesterone restores mitochondrial bioenergetic function in streptozotocin- and amyloid-β-challenged HT-22 hippocampal cells: An in vitro model of Alzheimer's disease
AU - Seema Yousuf
AU - Fahim Atif
AU - Donald G. Stein
PY - 2026
DA - 2026/10/27
JO - Journal of Alzheimer's Disease Reports
DO - 10.1177/25424823261498338
UR - https://doi.org/10.1177/25424823261498338
AB - Background Mitochondrial dysfunction contributes to Alzheimer's disease (AD) by promoting bioenergetic failure and neuronal loss. Objective We investigated whether progesterone (P4) protects against mitochondrial impairment in two in vitro AD models. Methods Mouse hippocampal HT-22 cells were exposed to amyloid-β (Aβ) or streptozotocin (STZ) and treated with P4. Mitochondrial respiration was assessed using Seahorse extracellular flux analysis. Results Both Aβ and STZ significantly reduced basal and maximal respiration, spare respiratory capacity, and ATP-linked respiration (ATP production rate), while increasing proton leak and cell death. P4 treatment restored mitochondrial respiratory parameters and improved cell viability. Conclusions These findings suggest progesterone preserves mitochondrial bioenergetic function under AD-related stress conditions.
SN - 2542-4823
ER -