Vascular cognitive impairment refers to a group of syndromes ranging from mild cognitive impairment to dementia caused by risk factors for cerebrovascular disease, dominant cerebrovascular disease, and non-dominant cerebrovascular disease. Vascular cognitive impairment is the second most common form of dementia**, accounting for about 20% of all dementia and second only to Alzheimer's disease. Unlike Alzheimer's disease, the occurrence of dementia can be controlled through early detection of early** vascular cognitive impairment, and even reach the clinical**. Ischemic vascular cognitive impairment is acute and chronic cognitive impairment caused by occlusion or hypoperfusion of large and small blood vessels, which is a common category of vascular cognitive impairment.
Ginkgolide injection is a natural medicine for ischemic stroke, and relevant basic studies have confirmed that it also has a regulatory effect on neurological abnormalities such as Alzheimer's disease, vascular cognitive impairment, and depression. Animal and in vitro studies have confirmed that the mechanism of ginkgolide injection in regulating cognitive function may be to improve vascular function, anti-oxidative stress, anti-neuronal apoptosis, etc.
There is a study to use ginkgolide injection** ischemic vascular cognitive impairment to observe the cognitive function and self-care ability of patients, and to detect serum superoxide dismutase (SOD) and glutathione (GSH) levels, aiming to evaluate the efficacy of ginkgolide injection and preliminarily ** its mechanism of action.
The occurrence of ischemic vascular cognitive impairment is inseparable from the decrease of cerebral blood flow, but the progression of cognitive dysfunction may not be alleviated by the improvement of cerebral blood flow status. Therefore, although restoring cerebral blood flow is the basic principle of ischemic vascular cognitive impairment, the effective means of improving cognitive function need further research.
In recent years, a large number of clinical studies have shown that even if the responsible blood vessels are recanalized or the aggravation of vascular lesions is effectively delayed by interventional surgery or drugs, the cognitive function and life ability of patients cannot be significantly improved, which is also a difficult problem in the current research and clinical development of vascular cognitive impairment. In addition, it has also been found that the efficacy of the use of cholinergic drugs** for vascular cognitive impairment is not satisfactory. These clinical phenomena may be due to the main pathological mechanism of the patient's cognitive dysfunction is the nerve damage caused by the lack of oxygen in the brain tissue caused by the blockage of blood vessels, even if the patency of the responsible blood vessels is restored or other blood vessels are compensated for the diseased brain tissue, the pathological changes such as apoptosis of nerve cells in the diseased brain tissue will not be significantly reversed due to the restoration of blood flow. Therefore, the discovery of targeted targets in the pathological mechanism of nerve cell damage in diseased brain tissue may be the key to improving patients' cognitive impairment.