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• Vol.52 No.11
• CLINICA NEUROL, 52: 908−910, 2012
• Vol.52 No.11 contents

Symposium 1

Molecular mechanism and new protective strategy for ischemic white matter damages

Takao Urabe, M.D., Ph.D.

Department of Neurology, Juntendo University Urayasu Hospital

Brain white matter lesions (WMLs), which are often observed in patients with ischemic cerebrovascular diseases, contribute to cognitive decline. We analyzed the pathologic and regenerative processes in brain white matter lesions of patients diagnosed with vascular dementia. There was a significant increase in the number of oligodendrocyte progenitor cells (OPCs) in the brains of patients with vascular dementia as well as in rats with cerebral hypoperfusion. WMLs can be induced experimentally by bilateral common carotid artery ligation (BCCAL) of rats to cause chronic cerebral ischemia. After chronic cerebral hypoperfusion injury, oxygen free radicals and activated microglia acting as inflammatory elements contribute to chronic cerebral hypoperfusion-induced WMLs. The cell death of oligodendrocytes (OLGs) contributes directly to WMLs. The activation for intracellular signaling pathway of cAMP responsive element binding protein (CREB) phosphorylation in the white matter was suppressed after BCCAL. Type III phosphodiesterase inhibitor (PDE3-I) has potential therapeutic and brain-protective effects based on multitarget mechanism through cell signaling pathway of CREB phosphorylation. The OPCs subsequently underwent cell death and the number of OLGs decreased. In the rat model, PDE3-I prevented cell death, markedly increased the mature OLGs, and promoted restoration of white matter and recovery of cognitive decline.
Full Text of this Article in Japanese PDF (232K)

(CLINICA NEUROL, 52: 908−910, 2012)
key words: Ischemic white matter damage, Chronic cerebral hypoperfusion, Oligodendrocyte progenitor cell, Intracellular signaling pathway, cAMP responsive element binding protein phosphorylation

(Received: 23-May-12)