Endothelial Progenitor Cells' Classification and Application in Neurological Diseases

The therapeutic effects of endothelial progenitor cells (EPCs) on ischemic stroke have been extensively studied in recent years. However, the differences in early EPCs and endothelial outgrowth cells (EOCs) are still unclear. Clarifications of their respective properties and specific functioning characteristics contribute to better applications of EPCs in ischemic diseases. In this review, we discuss cellular origin, isolation, culture, surface markers of early EPCs and EOCs and relevant applications in neurological diseases. We conclude that EOCs possess all haracteristics of true endothelial progenitors and have potent advantages in EPC-based therapies for ischemic diseases. A number of preclinical and clinical applications of EPCs in neurological diseases are under study. More studies are needed to determine the specific characteristics of EPCs and the relevant mechanisms of EPCs for neurological diseases.

Nerve growth factor for the treatment of spinocerebellar ataxia type 3: an open-label study / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Spinocerebellar ataxia type 3 (SCA3) is the most common subtype of SCA worldwide, and runs a slowly progressive and unremitting disease course. There is currently no curable treatment available. Growing evidence has suggested that nerve growth factor (NGF) may have therapeutic effects in neurodegenerative diseases, and possibly also in SCA3. The objective of this study was to test the efficacy of NGF in SCA3 patients.</p><p><b>METHODS</b>We performed an open-label prospective study in genetically confirmed adult (>18 years old) SCA3 patients. NGF was administered by intramuscular injection (18 μg once daily) for 28 days consecutively. All the patients were evaluated at baseline and 2 and 4 weeks after treatment using the Chinese version of the scale for assessment and rating of ataxia (SARA).</p><p><b>RESULTS</b>Twenty-one SCA3 patients (10 men and 11 women, mean age 39.14 ± 7.81 years, mean disease duration 4.14 ± 1.90 years, mean CAG repeats number 77.57 ± 2.27) were enrolled. After 28 days of NGF treatment, the mean total SARA score decreased significantly from a baseline of 8.48 ± 2.40 to 6.30 ± 1.87 (P < 0.001). Subsections SARA scores also showed significant improvements in stance (P = 0.003), speech (P = 0.023), finger chase (P = 0.015), fast alternating hand movements (P = 0.009), and heel-shin slide (P = 0.001).</p><p><b>CONCLUSIONS</b>Our preliminary data suggest that NGF may be effective in treating patients with SCA3.</p>

Effect of naloxone on aluminum-induced learning and memory impairment in rats.

BACKGROUND: Uptake of aluminum may disturb the learning and memory of humans or animals. Naloxone (NAL) has been shown to exert beneficial effects on memory deficits. AIMS: We investigated the effects of naloxone on aluminum-induced learning and memory impairment in rats. SETTINGS AND DESIGN: Aluminum-induced learning and memory impairment model was established by gavage of Aluminum chloride (600 mg/kg) for 3 months. Rats were divided into three groups viz. naloxone-treated rats (NAL 0.8 mg/kg, i.p. daily for 7 days), non-treated model rats and normal controls. MATERIALS AND METHODS: The Morris water maze test was performed to study spatial learning and memory. Long-term potentiation (LTP) of the Schaffer collateral-CA1 synapse was recorded. Aluminum and zinc contents in the hippocampus were assayed with atomic absorption spectrophotometry. STATISTICAL ANALYSIS: Parameters of the hidden and visible platform trials and data of LTP were analyzed using two-way repeated measures ANOVA. RESULTS: In the hidden platform trials, escape latencies of the NAL rats were significantly shorter than that of the non-treated rats (P=0.000, 95% confidential interval low bound 14.31, upper bound 22.68). In probe trails, the number of entries in the target area of the NAL rats (6.75+/-1.28 times/min) was more than that of non-treated model rats (4.56+/-2.16 times/min, P=0.004, 95% confidence interval low bound -3.65, upper bound -0.788). The magnitudes of LTP recorded in the CA1 pyramidal neurons of the NAL-treated rats were significantly augmented when compared to the non-treated model rats (P=0.005, 95% confidence interval low bound 0.16, upper bound 0.84). CONCLUSIONS: NAL could facilitate spatial learning and memory and enhance LTP in the CA1 region of the hippocampus in aluminum-induced learning and memory impairment in rats.

Effect of naloxone on cognitive function in vascular dementia in rats.

BACKGROUND & OBJECTIVES: The endogenous opioid system plays an important role in cognitive functions and may also contribute to the progression of some kind of dementia. Naloxone has been shown to exert beneficial effects on memory deficits in patients with senile dementia and reverse some of the effects induced by endogeneous opioids. We therefore investigated the effects of naloxone on cognitive function in rats with vascular dementia (VD). METHODS: Vascular dementia was established by permanent occlusion of the common carotid arteries. Rats were divided into three groups viz., sham-operated controls, naloxone treated VD rats (naloxone 0.8 mg/kg, i.p. daily for 7 days), and nontreated VD rats. The Morris water maze test was performed to study spatial learning and memory. The extracellular recording technique was used to record long-term potentiation (LTP) of the Schaffer collateral-CA1 synapse in the rat hippocampal slices. RESULTS: In the hidden platform trials, escape latencies of the naloxone treated VD rats were significantly shorter than that of the nontreated VD rats (P < 0.001). In the probe trials, the number of enteries in the target area of the naloxone treated VD rats (8.36 +/- 1.38 times/min) were more than that of the nontreated VD rats (4.64 +/- 1.73 times/min) (P < 0.01). The magnitudes of LTP recorded in the CA1 pyramidal neurons of the naloxone treated VD rats were significantly augmented when compared to the nontreated VD rats (P < 0.05). INTERPRETATION & CONCLUSION: Naloxone could facilitate spatial learning and memory and enhance LTP in the CA1 region of hippocampus in rats with VD. It is postulated that naloxone might exert beneficial effects on cognitive function in VD in rats by modulating the synaptic plasticity in the hippocampal neuronal network.