RTP801 regulates motor cortex synaptic transmission and learning.

Background: RTP801/REDD1 is a stress-regulated protein whose upregulation is necessary and sufficient to trigger neuronal death in in vitro and in vivo models of Parkinson's and Huntington's diseases and is up regulated in compromised neurons in human postmortem brains of both neurodegenerative disorders. Indeed, in both Parkinson's and Huntington's disease mouse models, RTP801 knockdown alleviates motor-learning deficits.

Results: We investigated the physiological role of RTP801 in neuronal plasticity and we found RTP801 in rat, mouse and human synapses.

Psychological Health and Physical Activity Levels during the COVID-19 Pandemic: A Systematic Review.

The coronavirus disease (COVID-19) pandemic has been devastating in all senses, particularly psychologically. Physical activity (PA) is known to aid psychological well-being, and it is worth investigating whether PA has been a coping strategy during this pandemic. The objective of this literature review is to analyze the extent to which engaging in PA during the COVID-19 pandemic impacts psychological health in the adult population.

M2 cortex-dorsolateral striatum stimulation reverses motor symptoms and synaptic deficits in Huntington's disease.

Huntington's disease (HD) is a neurological disorder characterized by motor disturbances. HD pathology is most prominent in the striatum, the central hub of the basal ganglia. The cerebral cortex is the main striatal afferent, and progressive cortico-striatal disconnection characterizes HD.

Adaptation of Camelus dromedarius pars nervosa of the hypophysis to winter and summer living conditions.

The aim of this work is to study the characteristics of the dromedary nervous lobe and determine how the seasons condition its organization. To this end, electron microscopy was performed and examined quantitatively on animals from winter and summer periods. The results show a higher number of cells in the nervous lobe in summer than in winter.

Dogs with cognitive dysfunction syndrome: a natural model of Alzheimer's disease.

In the search for appropriate models for Alzheimer's disease (AD) involving animals other than rodents, several laboratories are working with animals that naturally develop cognitive dysfunction. Among the animals tested, dogs are quite unique in helping to elucidate the cascade of events that take place in brain amyloid-beta (Aβ)deposition aging, and cognitive deficit. Recent innovative research has validated human methods and tools for the analysis of canine neuropathology and has allowed the development of two different approaches to investigate dogs as natural models of AD.

Magnetic resonance imaging of cerebral involutional changes in dogs as markers of aging: an innovative tool adapted from a human visual rating scale.

The dog is increasingly considered as a natural animal model for the study of normal and pathological human brain aging, because it exhibits anatomical, biochemical and cognitive changes that parallel those seen in humans. This study presents a novel visual semi-quantitative rating scale of canine cerebral magnetic resonance imaging (MRI). Ninety-eight dogs of both sexes from 27 pure breeds, aged 2-15 years, were used.

Canine cognitive dysfunction and the cerebellum: acetylcholinesterase reduction, neuronal and glial changes.

The specific functional and pathological alterations observed in Alzheimer's disease are less severe in the cerebellum than in other brain areas, particularly the entorhinal cortex and hippocampus. Since dense core amyloid-beta plaque formation has been associated with an acetylcholinesterase heterogeneous nucleator action, we examined if an acetylcholinesterase imbalance was involved in cerebellum plaque deposition. By using the canine counterpart of senile dementia of the Alzheimer's type, a promising model of human brain aging and early phases of Alzheimer's disease, we investigated how cerebellar pathology and acetylcholinesterase density could be related with cognitive dysfunction.