No abstract

Vascular dementia is a devastating disorder not only for the patient, but also for the family because this neurocognitive disorder breaks the patient's independence, and leads to family care of the patient with a high cost for the family. This complex disorder alters memory, learning, judgment, emotional control and social behavior and affects 4% of the elderly world population. The high blood pressure or arterial hypertension is a major risk factor for cerebrovascular disease, which in most cases leads to vascular dementia. Interestingly, this neurocognitive disorder starts after long lasting hypertension, which is associated with reduced cerebral blood flow or hypoperfusion, and complete or incomplete ischemia with cortical thickness. Animal models have been generated to elucidate the pathophysiology of this disorder. It is known that dendritic complexity determines the receptive synaptic contacts, and the loss of dendritic spine and arbor stability are strongly associated with dementia in humans. This review evaluates relevant data of human and animal models that have investigated the link between long-lasting arterial hypertension and neural morphological changes in the context of vascular dementia. We examined the effect of chronic arterial hypertension and aged in vascular dementia. Neural dendritic morphology in the prefrontal cortex and the dorsal hippocampus and nucleus accumbens after chronic hypertension was diskussed in the animal models of hypertension. Chronic hypertension reduced the dendritic length and spine density in aged rats.

The spontaneously hypertensive (SH) rat has been used as an animal model of vascular dementia (VD). Our previous report showed that, SH rats exhibited dendritic atrophy of pyramidal neurons of the CA1 dorsal hippocampus and layers 3 and 5 of the prefrontal cortex (PFC) at 8 months of age. In addition, we showed that cerebrolysin (Cbl), a neurotrophic peptide mixture, reduces the dendritic atrophy in aged animal models. This study aimed to determine whether Cbl was capable of reducing behavioral and neuronal alterations, in old female SH rats. The level of diastolic and systolic pressure was measured every month for the 6 first months and only animals with more than 160 mm Hg of systolic pressure were used. Female SH rats (6 months old) received 6 months of Cbl treatment. Immediately after the Cbl treatment, two behavioral tests were applied, the Morris water maze test for memory and learning and locomotor activity in novel environments. Immediately after the last behavioral test, dendritic morphology was studied with the Golgi-Cox stain procedure followed by a Sholl analysis. Clearly, SH rats with Cbl showed an increase in the dendritic length and dendritic spine density of pyramidal neurons in the CA1 in the dorsal hippocampus and layers 3 and 5 of the PFC. Interestingly, Cbl improved memory of the old SH rats. Our results support the possibility that Cbl may have beneficial effects on the management of brain alterations in an animal model with VD. Synapse 70:378-389, 2016. © 2016 Wiley Periodicals, Inc.

Malathion is a highly neurotoxic pesticide widely used in daily life. Acute and chronic toxicity from this organophosphorus compound may cause damage to health, especially to the central nervous system. In the present work, we show the effects of chronic exposure of malathion on dendritic morphology of neurons from prefrontal cortex (PFC), hippocampus, and nucleus accumbens (NAcc) in adult male mice. Animals were injected i.p. with low dose of malathion (40 mg/kg body weight) for 14 days. Control animals were injected with corn oil, used as vehicle. Fourteen days after the last injection, brains were removed and processed by the Golgi-Cox stain method, and coronal sections were obtained to perform Sholl analysis on pyramidal neurons from the PFC, CA1 area from the hippocampus, and medium spiny cells from the NAcc. Dendritic morphology analysis included the total dendritic length, the maximum branching order, and the dendritic spine density. Results indicated a significant decrement on dendritic morphology in neurons from the hippocampus and the PFC in animals injected with malathion, whereas medium spiny neurons from NAcc showed a significant decrement only on the dendritic spine density in malathion injected mice, as compared to control mice. These results suggest that chronic toxicity of malathion alters the dendritic morphology in adult age, which may affect behavior.

Diabetes mellitus (DM) is characterized by high levels of blood glucose. In recent years, its prevalence has increased, which was 422 million in the world in 2014. In elderly patients, DM is associated with deficits in memory and learning processes. The cognitive deficits lead to dementia. With the development of animal models in DM, it has been possible to better understand quantitative morphological changes in numerous neuronal structures belonging to the limbic system, such as the prefrontal cortex (PFC), the hippocampus and basolateral amygdala (BLA). These structures are in close relationship with processes of memory and learning. Several reports have demonstrated that chronic hyperglycemia reduces spinogenesis and dendritic arborization in the aforementioned regions along with a decline in memory and learning processes, especially in streptozotocin (STZ)‐induced diabetic rats. In the present review, we discuss animal models, the effects of chronic hyperglycemia on dendritic morphology of limbic regions and memory and learning processes, the effect on neural transmission in these regions, the pathologic mechanisms involved, and the relevance of dendritic morphology in diabetes. All of this information can help us to have a better understanding of dementia in diabetes mellitus and propose strategies for its prevention and treatment.