Early detection of memory deficits and memory improvement with vaccinia virus complement control protein in an Alzheimer's disease model.

Vaccinia virus complement control protein (VCP) inhibits both the classical and alternate complement pathways. In diseases such as traumatic brain injury (TBI) and Alzheimer's disease (AD), pathological inflammation is caused by amongst several factors, prolonged or inappropriate activation of the complement system and is a significant cause of neurodegeneration. This study investigates for the first time the use of a cheeseboard maze to evaluate cognitive deficits and the effect of VCP on memory processes in 2- and 3-month-old mice that express mutant amyloid precursor protein (APPswe) and mutant presenilin 1 (Ps1dE9) that correspond to a form of early onset AD.

Development of a mild prenatal stress rat model to study long term effects on neural function and survival.

Early development of the brain's neural circuitry has been shown to be vulnerable to high levels of circulating steroid hormones such as corticosterone. These steroid hormones are lipophylic and can cross the placental barrier especially during the last week of gestation leading to disturbances in the formation of neural circuits that contain amongst others dopaminergic and serotonergic neurons. The effects of this disruption of neuronal circuit formation during gestation has been shown to manifest in adult offspring as behavioural abnormalities such as anxiety and an abnormal hypothalamic-pituitary-adrenal (HPA) axis.

Vaccinia virus complement control protein significantly improves sensorimotor function recovery after severe head trauma.

Vaccinia virus complement control protein (VCP) is an immunomodulator that inhibits both the classical and alternate pathways of the complement system, therefore preventing cell death and inflammation. VCP has previously been shown to be therapeutically effective in mild and moderate traumatic brain injury models. In this study the efficacy of VCP in a severe head injury model is investigated in Wistar rats.

Administration of vaccinia virus complement control protein shows significant cognitive improvement in a mild injury model.

Previous studies have shown that traumatic mild brain injury in a rat model is accompanied by breakdown of the blood brain barrier and the accumulation of inflammatory cells. A therapeutic agent, vaccinia virus complement control protein (VCP), inhibits both the classic and the alternative pathways of the complement system and, in so doing, prevents cell death and inflammation. With the use of a rat mild injury model, the effects of VCP on spatial learning and memory were tested.

Herbal complement inhibitors in the treatment of neuroinflammation: future strategy for neuroprotection.

The upregulated complement system plays a damaging role in disorders of the central nervous system (CNS). The classical and alternate pathways are two major pathways activated in neuroinflammatory disorders such as Alzheimer's disease, multiple sclerosis, traumatic brain injury, spinal cord injury, HIV-associated dementia, Parkinson's disease, and mad cow disease. Failure of currently available anti-inflammatory agents, especially cyclooxygenase inhibitors, in offering significant neuroprotection in large epidemiologic clinical trials of CNS disorders suggests an urgent need for the development of new neuroprotective agents.

Molecular mechanisms, emerging etiological insights and models to test potential therapeutic interventions in Alzheimer's disease.

Alzheimer's disease (AD) is a common cause of dementia, resulting from accumulated beta-amyloid protein deposits in the brain. As the population ages the incidence of AD is also on the rise. The incidence is very high in the developed countries where life expectancy is high, but it is also rising rapidly in the developing countries.

Neuroprotection from complement-mediated inflammatory damage.

Several neurodegenerative disorders, such as multiple sclerosis, Alzheimer's disease, and Parkinson's disease, are associated with inflammatory damage. The complex process of neuroinflammation involves various components of the immune system and the central nervous system. Particularly, brain astrocytes and microglial cells generate several inflammatory mediators like cytokines, leukotrienes, superoxide radicals, eicasonoids, and the components of the complement cascade.