Ovariectomy and High Fat-Sugar-Salt Diet Induced Alzheimer's Disease/Vascular Dementia Features in Mice.

While the vast majority of Alzheimer's disease (AD) is non-familial, the animal models of AD that are commonly used for studying disease pathogenesis and development of therapy are mostly of a familial form. We aimed to generate a model reminiscent of the etiologies related to the common late-onset Alzheimer's disease (LOAD) sporadic disease that will recapitulate AD/dementia features. Naïve female mice underwent ovariectomy (OVX) to accelerate aging/menopause and were fed a high fat-sugar-salt diet to expose them to factors associated with increased risk of development of dementia/AD.

Predisposition to cortical neurodegenerative changes in brains of hypertension prone rats.

Background: Substantial evidence suggests that hypertension is a significant risk factor for cognitive decline. However, it is unclear whether the genetic predisposition to hypertension is also associated with cellular dysfunction that promotes neurodegeneration.

Methods: Changes in blood pressure were evaluated following dietary salt-loading or administration of a regular diet in Sabra Normotensive (SBN/y) and Sabra Hypertension-prone rats (SBH/y).

New Cortical Neurodegenerative Pathways in the Hypertensive Rat Brain.

Hypertension is a risk factor for neurodegenerative diseases. We hypothesized that chronic hypertension underlies neurodegeneration. In this study, we examined the expression of brain cortical proteins involved in homeostasis, apoptosis, and brain functions in Spontaneously Hypertensive Rats (SHR) compared with normotensive Wistar-Kyoto (WKY) rats.

[INVOLVEMENT OF EPIGENETIC REGULATION IN CEREBRAL CELL DEATH FOLLOWING TRAUMATIC BRAIN INJURY IN A RAT MODEL].

Introduction: Traumatic brain injuries (TBI) are a major cause of mortality and disability among young adults. TBI are characterized by primary injury, the result of a mechanical impact to the cranium and a secondary injury, a series of molecular mechanism processes developing thereafter. Cerebral cells modify their gene and protein expression as a result of the injury.