Publications by authors named "Kristi McConnell"

Background: The nucleus accumbens (NAc) plays a key role in brain reward processes including drug seeking and reinstatement. Several anatomical, behavioral, and neurochemical studies discriminate between the limbic-associated shell and the motor-associated core regions. Less studied is the fact that the shell can be further subdivided into a dorsomedial shell (NAcDMS) and an intermediate zone (NAcINT) based on differential expression of transient c-Fos and long-acting immediate-early gene ΔFosB upon cocaine sensitization.

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Background: Huntington's disease (HD) is characterized not only by severe motor deficits but also by early cognitive dysfunction that significantly increases the burden of the disease for patients and caregivers. Considerable efforts have concentrated, therefore, on the assessment of cognitive deficits in some HD mouse models. However, many of these models that exhibit cognitive deficits also have contemporaneous serious motor deficits, confounding interpretation of cognitive decline.

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Huntington's disease (HD) is an autosomal dominant, progressive neurodegenerative disorder caused by expansion of CAG repeats in the huntingtin gene. Tissue transglutaminase 2 (TG2), a multi-functional enzyme, was found to be increased both in HD patients and in mouse models of the disease. Furthermore, beneficial effects have been reported from the genetic ablation of TG2 in R6/2 and R6/1 mouse lines.

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The genome of the Bacterial Artificial Chromosome (BAC) transgenic mouse model of Huntington's Disease (BAC HD) contains the 170 kb human HTT locus modified by the addition of exon 1 with 97 mixed CAA-CAG repeats. BAC HD mice present robust behavioral deficits in both the open field and the accelerating rotarod tests, two standard behavioral assays of motor function. BAC HD mice, however, also typically present significantly increased body weights relative to wildtype littermate controls (WT) which potentially confounds the interpretation of any motor deficits associated directly with the effects of mutant huntingtin.

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Article Synopsis
  • Huntington's disease (HD) is a hereditary neurodegenerative disorder with motor, cognitive, and psychiatric symptoms, caused by an expansion of CAG repeats in the huntingtin gene.
  • Researchers have developed the zQ175 knock-in mouse model, which has a higher CAG repeat length than previous models, leading to more pronounced symptoms and earlier onset of behavioral deficits.
  • The study found that both heterozygous and homozygous zQ175 mice showed significant motor and cognitive impairments, weight loss, and reduced survival, indicating the model's potential for studying HD progression and therapeutic approaches.
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Background: Sex hormones play a significant role in human physiology. Estrogen may have protective effects in the cardiovascular system, as evidenced by the decreased incidence of cardiovascular disease (CVD) in premenopausal compared with postmenopausal women.

Objective: This review highlights the acute and long-term effects of sex hormones on the vascular endothelium and vascular smooth muscle (VSM) in adults.

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