Exploring the Therapeutic Potential of Benfotiamine in a Sporadic Alzheimer's-Like Disease Rat Model: Insights into Insulin Signaling and Cognitive function.

Alzheimer's disease (AD) is a complex neurodegenerative process, also considered a metabolic condition due to alterations in glucose metabolism and insulin signaling pathways in the brain, which share similarities with diabetes. This study aimed to investigate the therapeutic effects of benfotiamine (BFT), a vitamin B1 analog, in the early stages of the neurodegenerative process in a sporadic model of Alzheimer's-like disease induced by intracerebroventricular injection of streptozotocin (STZ). Supplementation with 150 mg/kg of BFT for 7 days reversed the cognitive impairment in short- and long-term memories caused by STZ in rodents.

Use of Hormone Therapy in Postmenopausal Women with Alzheimer's Disease: A Systematic Review.

Background: Around two-thirds of patients with Alzheimer's disease (AD) are women, which could be related to the depletion of female sexual hormones at menopause. The replacement of these hormones with hormone therapy (HT) to possibly decrease AD risk or treat AD patients has generated conflicting results in the literature.

Objective: Our aim was to systematically review the relationship between HT use in postmenopausal women with AD and the risk of developing or treating AD symptoms.

Cannabinoid Receptor Type 1 Agonist ACEA Improves Cognitive Deficit on STZ-Induced Neurotoxicity Through Apoptosis Pathway and NO Modulation.

The cannabinoid system has the ability to modulate cellular and molecular mechanisms, including excitotoxicity, oxidative stress, apoptosis, and inflammation, acting as a neuroprotective agent, by its relationship with signaling pathways associated to the control of cell proliferation, differentiation, and survival. Recent reports have raised new perspectives on the possible role of cannabinoid system in neurodegenerative diseases like Alzheimer disease's (AD). AD is a neurodegenerative disorder characterized by the presence of amyloid plaques, neurofibrillary tangles, neuronal death, and progressive cognitive loss, which could be caused by energy metabolism impairment, changes in insulin signaling, chronic oxidative stress, neuroinflammation, Tau hyperphosphorylation, and Aβ deposition in the brain.

Cannabinoid Receptor Type 1 Agonist ACEA Protects Neurons from Death and Attenuates Endoplasmic Reticulum Stress-Related Apoptotic Pathway Signaling.

Neurodegeneration is the result of progressive destruction of neurons in the central nervous system, with unknown causes and pathological mechanisms not yet fully elucidated. Several factors contribute to neurodegenerative processes, including neuroinflammation, accumulation of neurotoxic factors, and misfolded proteins in the lumen of the endoplasmic reticulum (ER). Endocannabinoid signaling has been pointed out as an important modulatory system in several neurodegeneration-related processes, inhibiting the inflammatory response and increasing neuronal survival.

Temporal changes of CB1 cannabinoid receptor in the basal ganglia as a possible structure-specific plasticity process in 6-OHDA lesioned rats.

The endocannabinoid system has been implicated in several neurobiological processes, including neurodegeneration, neuroprotection and neuronal plasticity. The CB1 cannabinoid receptors are abundantly expressed in the basal ganglia, the circuitry that is mostly affected in Parkinson's Disease (PD). Some studies show variation of CB1 expression in basal ganglia in different animal models of PD, however the results are quite controversial, due to the differences in the procedures employed to induce the parkinsonism and the periods analyzed after the lesion.

Different approaches, one target: understanding cellular mechanisms of Parkinson's and Alzheimer's diseases.

Neurodegenerative disorders are undoubtedly an increasing problem in the health sciences, given the increase of life expectancy and occasional vicious life style. Despite the fact that the mechanisms of such diseases are far from being completely understood, a large number of studies that derive from both the basic science and clinical approaches have contributed substantial data in that direction. In this review, it is discussed several frontiers of basic research on Parkinson's and Alzheimer's diseases, in which research groups from three departments of the Institute of Biomedical Sciences of the University of São Paulo have been involved in a multidisciplinary effort.

Early and late neurodegeneration and memory disruption after intracerebroventricular streptozotocin.

Glucose metabolism and insulin signaling disruptions in the brain have been proposed as a likely etiology of Alzheimer's disease. The aim of the present study was to investigate the time course of cognitive impairments induced by intracerebroventricular injection of streptozotocin (STZ) in rats and correlate them with the ensuing neurodegenerative process. Early and late effects of STZ were evaluated by using the reference and working memory versions of the Morris' water maze task and the evaluation of neurodegenerative markers by immunoblotting and the Fluoro-Jade C histochemistry.

Hypoactivity of the central dopaminergic system and autistic-like behavior induced by a single early prenatal exposure to lipopolysaccharide.

The aim of the present study was to evaluate the behavioral patterns associated with autism and the prevalence of these behaviors in males and females, to verify whether our model of lipopolysaccharide (LPS) administration represents an experimental model of autism. For this, we prenatally exposed Wistar rats to LPS (100 μg/kg, intraperitoneally, on gestational day 9.5), which mimics infection by gram-negative bacteria.

Differential response of AMPA and NMDA glutamate receptors of Purkinje cells to aging of the chicken cerebellum.

Aging can lead to cognitive, affective, learning, memory and motor deficits. Since the cerebellum and glutamatergic neurotransmission are involved in several of those functions, the present work aimed at studying the expression of AMPA and NMDA glutamate receptor subunits in the chick cerebellum during aging. Young (30 days old) and aged (ca.

Retinal removal up-regulates cannabinoid CB(1) receptors in the chick optic tectum.

The endocannabinoid system has been implicated in several neurobiological processes, including neurodegeneration and neuroprotection. The aim of this study was to evaluate the effects of unilateral retinal ablation on the expression of the cannabinoid receptor subtype 1 (CB(1)) at both protein and mRNA levels in the optic tectum of the adult chick brain. After different survival times postlesion (2-30 days), the chick brains were subjected to immunohistochemical, immunoblotting, and real-time PCR procedures to evaluate CB(1) expression.

ERK3 associates with MAP2 and is involved in glucose-induced insulin secretion.

The adaptation of pancreatic islets to pregnancy includes increased beta cell proliferation, expansion of islet mass, and increased insulin synthesis and secretion. Most of these adaptations are induced by prolactin (PRL). We have previously described that in vitro PRL treatment increases ERK3 expression in isolated rat pancreatic islets.

Developmental expression of cannabinoid receptors in the chick retinotectal system.

The cannabinoid system has been suggested to participate in processes such as antinociception, cognition, motor control, and, more recently, development of the nervous system. This study describes the expression of the CB1 cannabinoid receptor in the developing chick retina and optic tectum by means of conventional immunoperoxidase protocols. CB1 immunoreactivity was initially detected around the embryonic day 4 (E4) in both the retina and tectum.

Increased expression of nitric oxide synthase in visual structures of the chick brain after retinal removal.

Nitric oxide (NO) seems to act as a retrograde messenger in the establishment and refinement of synaptic connections during development and in neural plasticity processes in adult life. Previous studies have shown that the expression of NO synthase (NOS) in the optic tectum of developing chicks is regulated by the retinal innervation. The aim of this study was to observe the effects of unilateral retinal lesions upon the expression of NOS in central visual areas of the adult chick brain.

Nicotine and alpha-bungarotoxin modify the dendritic growth of cholinoceptive neurons in the developing chick tectum.

Nicotinic acetylcholine receptors have been suggested to participate in morphogenetic processes during development of the nervous system. In this study, nicotine applied both in ovo and in vitro produced a reduction of the neuritic length of cholinoceptive neurons of the developing chick tectum, whereas alpha-bungarotoxin produced the opposite effect. Taken together with previous data, our results are indicative of a role of the alpha-bungarotoxin-sensitive nicotinic receptors in neural development.

Application of potassium chloride to the surface of the rat visual cortex differentially affects the expression of presumptive neuroprotective molecules.

The purpose of this study was to investigate the effects of topical application of 3 M KCl for 20 minutes to the surface of the rat visual cortex upon the expression of presumptive neuroprotective molecules. Conventional immunohistochemical and immunoblotting techniques revealed a marked reduction of the expression of calbindin and parvalbumin after application of KCl, whereas calretinin, nitric oxide synthase, and the alpha7 subunit of the nicotinic acetylcholine receptor clearly increased following that procedure. Such effects were quantified both in terms of the number of immunoreactive perikarya and optical density of immunoblottings, and were observed as soon as 1 h, and to last at least until 15 days, following KCl application.

Neurotransmitter regulation of neural development: acetylcholine and nicotinic receptors.

Several neurotransmitter systems have been related to developmental processes during the past decade. In this review, we discuss the evidence that the nicotinic acetylcholine receptors could have an additional function during development that may be unrelated to their role in cholinergic neurotransmission in the vertebrate brain. Both temporal expression data and in vitro and in vivo studies with nicotinic agonists and antagonists have provided direct support for a role of nicotinic receptors in neural developmental processes such as neurite outgrowth and differentiation.