Modeling of age-related neurological disease: utility of zebrafish.

Many age-related neurological diseases still lack effective treatments, making their understanding a critical and urgent issue in the globally aging society. To overcome this challenge, an animal model that accurately mimics these diseases is essential. To date, many mouse models have been developed to induce age-related neurological diseases through genetic manipulation or drug administration. These models help in understanding disease mechanisms and finding potential therapeutic targets. However, some age-related neurological diseases cannot be fully replicated in human pathology due to the different aspects between humans and mice. Although zebrafish has recently come into focus as a promising model for studying aging, there are few genetic zebrafish models of the age-related neurological disease. This review compares the aging phenotypes of humans, mice, and zebrafish, and provides an overview of age-related neurological diseases that can be mimicked in mouse models and those that cannot. We presented the possibility that reproducing human cerebral small vessel diseases during aging might be difficult in mice, and zebrafish has potential to be another animal model of such diseases due to their similarity of aging phenotype to humans.

Dimension-based quantification of aging-associated cerebral microvasculature determined by optical coherence tomography and two-photon microscopy.

Cerebral microvascular health is a key biomarker for the study of natural aging and associated neurological diseases. Our aim is to quantify aging-associated change of microvasculature at diverse dimensions in mice brain. We used optical coherence tomography (OCT) and two-photon microscopy (TPM) to obtain nonaged and aged C57BL/6J mice cerebral microvascular images in vivo. Our results indicated that artery & vein, arteriole & venule, and capillary from nonaged and aged mice showed significant differences in density, diameter, complexity, perimeter, and tortuosity. OCT angiography and TPM provided the comprehensive quantification for arteriole and venule via compensating the limitation of each modality alone. We further demonstrated that arteriole and venule at specific dimensions exhibited negative correlations in most quantification analyses between nonaged and aged mice, which indicated that TPM and OCT were able to offer complementary vascular information to study the change of cerebral blood vessels in aging.

Analysis and manegement of laminar blood flow inside a cerebral blood vessel using a finite volume software program for biomedical engineering.

BACKGROUND AND OBJECTIVE: Hemodynamic blood flow analysis in the cerebrovascular is has become one of the important research topics in the bio-mechanic in recent decades. The primary duty of the cerebral blood vessel is supplying Glucose and oxygen for the brain. METHODS: In this investigation, the non-Newtonian blood flow in the cerebral blood vessels studied. For modeling the geometry of this problem, we used Magnetic Resonance Image (MRI) approach to take Digital Imaging and Communications in Medicine (DICOM) images and using an open-source software package to construct the geometry, which is a complicated one. The power-law indexes, heat flux, and Reynolds number range in the investigation are 0.6 ≤ n ≤ 0.8, 5 ≤ q ≤ 15Wm-2 and 160≤Re≤310. Effects of Reynolds number, power-law indexes and heat fluxes are investigated. RESULTS: We found that the pressure drop increase with increasing the Reynolds number and power-law index. The maximum Nusselt number in the cerebral blood vessels accrued in the running position of the body in n = 0.8. Also, the highest average wall shear stress occurs in maximum power-law indexes and Reynolds number. CONCLUSION: By increasing the power-law index and Reynolds number, the wall shear stress increases.

Cerebral blood vessel damage in traumatic brain injury.

Traumatic brain injury is a devastating cause of death and disability. Although injury of brain tissue is of primary interest in head trauma, nearly all significant cases include damage of the cerebral blood vessels. Because vessels are critical to the maintenance of the healthy brain, any injury or dysfunction of the vasculature puts neural tissue at risk. It is well known that these vessels commonly tear and bleed as an immediate consequence of traumatic brain injury. It follows that other vessels experience deformations that are significant though not severe enough to produce bleeding. Recent data show that such subfailure deformations damage the microstructure of the cerebral vessels, altering both their structure and function. Little is known about the prognosis of these injured vessels and their potential contribution to disease development. The objective of this review is to describe the current state of knowledge on the mechanics of cerebral vessels during head trauma and how they respond to the applied loads. Further research on these topics will clarify the role of blood vessels in the progression of traumatic brain injury and is expected to provide insight into improved strategies for treatment of the disease.