Electroacupuncture Ameliorates Cognitive Impairment in Vascular Dementia Rats
An incredibly involved and detailed paper. Using a simple acupuncture combination of points they were able to show that acupuncture alleviates the cognitive impairment caused by a model of vascular dementia. pdf of the study at this link Electroacupuncture Ameliorates Cognitive Impairment in Vascular Dementia Rats Brain and Behavior – 2026 – Guo
As usual, for me the issue is dosage. How can we practically achieve the same dosage of acupuncture as in these mice studies? In this study, they received 20 minutes of acupuncture q day for 21 days. This would not be impossible to do in humans if they were inpatients. But it, again, makes me think we should be doing acupuncture more frequently. That should be the expectation. Instead of what people will put up with. Then again, perhaps something wearable for a treatment as simple as this one would work too.
The citokines they studied (IL-1β, IL-6, and TNF-α) were ones I covered in my book, Radical Resilience
Guo, S., Q. Liu, S. Lin, T. Zhou, Q. Hu, and Z. Tang. 2026. “Electroacupuncture Ameliorates Cognitive Impairment in Vascular Dementia Rats: Potential Involvement of the Astrocyte–Synapse Axis.” Brain and Behavior16, no. 6: e71537. https://doi.org/10.1002/brb3.71537
ABSTRACT
Electroacupuncture Amelieorates Cognitive Impairment in Vascular Dementia Rats Introduction
This study investigated whether electroacupuncture at “Zhisanzhen” (EA-ZSZ) [this is combination of DU24 and bilateral GB13] alleviates cognitive impairment in vascular dementia (VD) rats by regulating the astrocyte–synapse axis, reshaping the hippocampal secretory microenvironment, and preserving synaptic structural integrity.
Methods Electroacupuncture
Sprague-Dawley rats were divided into sham, VD, VD+EA, and VD+Nim (nimodipine) groups. The VD model was established via a modified bilateral common carotid artery occlusion (2-VO). After 21 days, learning and memory were evaluated using the Morris water maze. Hippocampal CA1 histopathology and ultrastructure were assessed by H&E and transmission electron microscopy (TEM). RNA-seq identified differentially expressed genes (DEGs) and pathways. GFAP, BDNF, bFGF, and cytokines (IL-1β, IL-6, and TNF-α) were measured via immunofluorescence, Western blot, and ELISA.
Results
Compared to sham group, VD rats exhibited cognitive impairment, neuronal disorganization, and synaptic disruption. EA-ZSZ markedly alleviated cognitive deficits, outperforming nimodipine in spatial learning/memory, and restored synaptic ultrastructure (showing clearer clefts and increased vesicle abundance on TEM). RNA-seq showed that EA-ZSZ normalized pathways associated with cytokine-cytokine receptor interactions and synaptic signaling, restoring key “reversal genes” (Mdk, Homer1, and Npas4). These changes were accompanied by reduced GFAP, upregulated hippocampal BDNF/bFGF, and suppressed systemic cytokines (IL-1β, IL-6, and TNF-α).
Conclusion
EA-ZSZ exerts significant neuroprotective effects in VD rats by modulating the astrocyte–synapse axis, suppressing neuroinflammation, and enhancing neurotrophic/structural support within the hippocampal microenvironment. This highlights its multi-target advantage over monotherapies in repairing damaged synaptic architecture, supporting its clinical use.