Cerebral chronic hypoperfusion in mice causes premature aging of the cerebrovasculature.

Chronic cerebral hypoperfusion (CCH) is the main characteristic of an aged brain showing cerebrovascular alterations. Our previous study that the morphological changes in the pial arteries accompany a decrease in the cerebral blood flow in aged mouse brains, and it raises the question of whether artificial CCH can induce the same changes in brain vessel morphology. Here, we examined the effect of CCH on cerebrovascular morphology. Using a microcoil-induced chronic cerebral hypoperfusion (MCH) model, we induced CCH for 8 and 12 weeks. The cerebrovasculature morphology was evaluated using three-dimensional vessel analysis and compared with that of aging mice. We found the morphological changes in brain vessels of MCH mice, indicating that the CCH can induce cerebrovascular alteration. However, the changes in brain vessel morphology in the MCH mice were different in detail from those in the aging mice. Aging mice showed an increase in vessel tortuosity and thinned string vessels; MCH mice mainly showed thinned string vessels. This suggests that CCH may be a cause of age-related cerebrovascular alterations.

Effects of cerebral hypoperfusion on the cerebral white matter: a meta­analysis.

Decreased cerebral blood flow (CBF) in aging is known to induce aging­related cerebral deteriorations, such as neuronal degeneration, white matter (WM) alterations, and vascular deformations. However, the effects of cerebral hypoperfusion on WM alterations remain unclear. This study investigates the relationship between cerebral hypoperfusion and WM total volume changes by assessing the trends in CBF and WM changes by meta­analysis. In this meta­analysis, the differences in CBF were compared according to cerebral hypoperfusion type and the effect of cerebral hypoperfusion on the total volume of WM changes in rodents. Using subgroup analysis, 13 studies were evaluated for comparing CBF according to the type of cerebral hypoperfusion; 12 studies were evaluated for comparing the effects of cerebral hypoperfusion on the total volume of WM changes. Our meta­analysis shows that the total volume of WM decreases with a decrease in CBF. However, the reduction in\r\nthe total volume of WM was greater in normal aging mice than in the cerebral hypoperfusion model mice. These results suggest that the reduction of cerebral WM volume during the aging process is affected by other factors in addition to a decrease in CBF.

Unexpected Rearrangement of N-Allyl-2-phenyl-4,5-Dihydrooxazole-4-Carboxamides to Construct Aza-Quaternary Carbon Centers.

The unexpected rearrangement of N-allyl-2-phenyl-4,5-dihydrooxazole-4-carboxamides in the presence of LiHMDS has been found. The key features are: (1) the net reaction consisted of 1,3-migration of the N-allyl group, (2) the rearrangement produced a congested aza-quaternary carbon center, (3) both cyclic and acyclic substrates underwent the unexpected rearrangement to afford products in moderate to high yields, and (4) the reaction seemed to be highly stereoselective. In addition, a plausible mechanism has been discussed.

Role of hydrogen sulfide in cerebrovascular alteration during aging.

Hydrogen sulfide (H2S), a gasotransmitter molecule, has attracted attention as an endogenous signaling molecule because of its various pathological and physiological effects, including pathologies related to aging. In this review, we aimed to discuss the morphological changes in each vessel following aging, and to evaluate the possible role of H2S in the cerebrovascular alteration, such as arterial stiffness, microvessel loss, and blood-brain barrier disruption, with advancing age. Additionally, the review outlines the therapeutic efficacy of the H2S-releasing compounds on the cerebrovasculature. In the central nervous system, cerebrovascular aging can lead to the loss of blood-brain integrity, which causes cognitive impairment. The findings discussed in this review strongly support the notion that H2S has a potential therapeutic role in cerebrovascular alteration in aging.