Caveolin-1 and MLRs: A potential target for neuronal growth and neuroplasticity after ischemic stroke

You'll have to ask your doctor if anything in this review is worth creating an interventional protocol for. Hopefully you have a doctor who is responsible enough to actually go beyond the status quo and solve stroke. 

Did your doctor do anything with this earlier research on caveolin-1?

Treadmill exercise ameliorates focal cerebral ischemia/reperfusion-induced neurological deficit by promoting dendritic modification and synaptic plasticity via upregulating caveolin-1/VEGF signaling pathways December 2018 

San Diego Team Combats Memory Loss by Enhancing Brain Function 

October 2015

The latest here:

Caveolin-1 and MLRs: A potential target for neuronal growth and neuroplasticity after ischemic stroke

Wei Zhong1 ,  Qianyi Huang1,  Liuwang Zeng1, Zhiping Hu1, Xiangqi Tang1*

1 Department of Neurology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China

*Corresponding Author: Xiangqi Tang 
Department of Neurology, The Second Xiangya Hospital of Central South University, 
Renmin Road 139#, Changsha ,Hunan 410011, China.    
Tel:+86 13875807186   Fax: 0731-84896038   Email: txq6633@csu.edu.cn

 Abstract

Ischemic stroke is a leading cause of morbidity and mortality worldwide. Thrombolytic therapy, the only established treatment to reduce the neurological deficits caused by ischemic stroke, is limited by time window and potential complications. Therefore, it is necessary to develop new therapeutic strategies to improve neuronal growth and neurological function following ischemic stroke. Membrane lipid rafts (MLRs) are crucial structures for neuron survival and growth signaling pathways. Caveolin-1 (Cav-1), the main scaffold protein present in MLRs, targets many neural growth proteins and promotes growth of neurons and dendrites. Targeting Cav-1 may be a promising therapeutic strategy to enhance neuroplasticity after cerebral ischemia. This review addresses the role of Cav-1 and MLRs in neuronal growth after ischemic stroke, with an emphasis on the mechanisms by which Cav-1/MLRs modulate neuroplasticity via related receptors, signaling pathways, and gene expression. We further discuss how Cav-1/MLRs may be exploited as a potential therapeutic target to restore neuroplasticity after ischemic stroke. Finally, several representative pharmacological agents known to enhance neuroplasticity are discussed in this review.