डिमेंशिया का जर्नल

खुला एक्सेस

हमारा समूह 1000 से अधिक वैज्ञानिक सोसायटी के सहयोग से हर साल संयुक्त राज्य अमेरिका, यूरोप और एशिया में 3000+ वैश्विक सम्मेलन श्रृंखला कार्यक्रम आयोजित करता है और 700+ ओपन एक्सेस जर्नल प्रकाशित करता है जिसमें 50000 से अधिक प्रतिष्ठित व्यक्तित्व, प्रतिष्ठित वैज्ञानिक संपादकीय बोर्ड के सदस्यों के रूप में शामिल होते हैं।

ओपन एक्सेस जर्नल्स को अधिक पाठक और उद्धरण मिल रहे हैं
700 जर्नल और 15,000,000 पाठक प्रत्येक जर्नल को 25,000+ पाठक मिल रहे हैं

अमूर्त

Ischemic Vascular Dementia is an Overwhelming Threat for Elderly Individuals

Nicholas L Miller

Chronic cerebral hypoperfusion can cause dynamic demyelination as well as ischemic vascular dementia;in any case no successful medicines are accessible. Here, based on attractive reverberation imaging considers of patients with white matter harm, we found that this harm is related with disorganized cortical structure. In a mouse demonstrate, ontogenetic enactment of Glutamatergic neurons within the somatosensory cortex altogether advanced oligodendrocyte begetter cell (OPC) multiplication, remyelination within the corpus callosum, and recuperation of cognitive capacity after cerebral hypoperfusion. The helpful impact of such incitement was limited to the upper layers of the cortex, but too crossed a wide time window after ischemia. Mechanistically, upgrade of glutamatergic neuron-OPC useful synaptic associations is required to realize the security impact of enacting cortical glutamatergic neurons. Also,skin stroking, an simpler strategy to decipher into clinical hone, actuated the somatosensory cortex, in this manner advancing OPC expansion, remyelination and cognitive recuperation taking after cerebral hypoperfusion. In outline,we demonstrated that actuating glutamatergic neurons within the somatosensory cortex advances the multiplication of OPCs and remyelination to recuperate cognitive work after inveterate cerebral hypoperfusion. It ought to be famous that this actuation may give unused approaches for treating ischemic vascular dementia through the exact control of glutamatergic neuron-OPC circuits.