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High-dose 1,25-dihydroxyvitamin D supplementation elongates the lifespan of Huntington’s disease transgenic mice

100%

Molnar M. F., Torok R., Szalardy L., Sumegi E., Vecsei L., Klivenyi P.

Acta Neurobiologiae Experimentalis

2016

tom 76

nr 3

Huntington’s disease is an autosomal dominant progressive neurodegenerative disease, which results in a decreased quality of life and an early death. A high prevalence of vitamin D deficiency was first described in a 2013 study in patients with manifest Huntington’s disease, where serum vitamin D level was found to be associated with motor capabilities of the patients. Objectives: Our objective was to investigate the effect of a high-dose vitamin D3 supplementation on a transgenic mouse model of Huntington’s disease. Methods: Our study was performed on N171-82Q Huntington’s disease transgenic mice in age- and gender-matched groups. We collected data on the motor state and survival of the mice. Results: The results demonstrate that though vitamin D3 had no effect on the motor performance of transgenic mice, but significantly increased the lifespan of transgenic animals (Kaplan-Meier survival curves: vehicle-supplemented group: 73 (67–94) days vs. vitamin D3-supplemented group: 101 (74–109) days, p=0.048 Mantel-Cox log rank test). Conclusions: Further investigations are needed to determine whether a neuroprotective or a general corroborative effect of vitamin D leads to the measured effect. Our findings support the potential influence of vitamin D deficiency on the disease course and propose that vitamin D may be an effective supplementary treatment to beneficially influence clinical features of Huntington’s disease.

Evans Blue fluorescence permits the rapid visualization of non-intact cells in the perilesional rim of cold-injured rat brain

84%

Rakos G., Kis Z., Nagy D., Lur G., Farkas T., Hortobagyi T., Vecsei L., Toldi J.

Acta Neurobiologiae Experimentalis

2007

tom 67

nr 2

A focal cold lesion-induced injury, i.e., a model of focal vasogenic brain edema, enhances the permeability of the blood-brain barrier and cell membrane in the perilesional rim. However, non-intact cells can be detected, e.g. by markers of apoptosis, only hours or even days after the injury. The early membrane dysfunction allows extravasated serum proteins to enter the injured cells, which can be readily visualized if the plasma albumin was previously bound to fluorescent tracers, such as Evans Blue (EB). The aim of this study was to demonstrate injured cells that take up the EB/albumin conjugate in the perilesional rim. This tracer was administered 3.5 h after the induction of the injury and the animals were sacrificed 30 min later. With an excitation wavelength of 530–550 nm, the EB-positive cells emitted bright-red fluorescence at >590 nm and were easy to count. No positive cells were observed in the controls. This method provides more information than the classical 2,3,5-triphenyltetrazolium chloride reaction, because it permits an assessment of the density and distribution of cells with non-intact cell membranes in the perilesional area following cerebrocortical injury.

Ograniczanie wyników

2 Acta Neurobiologiae Experimentalis

2 Vecsei L.

1 Farkas T.

1 Hortobagyi T.

1 Kis Z.

1 Klivenyi P.

1 Lur G.

1 Molnar M. F.

1 Nagy D.

1 Rakos G.

1 Sumegi E.

1 Szalardy L.

1 Toldi J.

1 Torok R.

1 2016

1 2007

Wyniki wyszukiwania

High-dose 1,25-dihydroxyvitamin D supplementation elongates the lifespan of Huntington’s disease transgenic mice

Evans Blue fluorescence permits the rapid visualization of non-intact cells in the perilesional rim of cold-injured rat brain