Online scientific research on placentophagy: a bibliometric analysis.

Objective: To classify the bibliometric indicators of online scientific research on placentophagy.

Methods: A bibliometric study was conducted to quantify the scientific production of authors and institutions with the aim of highlighting the growth and impact of these publications nationally and internationally. The Bradford Law, network maps, and textual statistics were used, with searches conducted in libraries and databases in October 2021.

Integrative and complementary practices to control nausea and vomiting in pregnant women: a systematic review.

Objective: to synthesize the evidence available in the literature on the effects of integrative and complementary practices in nausea and vomiting treatment in pregnant women.

Method: a systematic review, reported according to PRISMA and registered in PROSPERO. The search for studies was carried out in 11 databases.

Neuronal Rubicon Represses Extracellular APP/Amyloid β Deposition in Alzheimer's Disease.

Alzheimer's disease (AD) is the most prevalent age-associated neurodegenerative disease. A decrease in autophagy during aging contributes to brain disorders by accumulating potentially toxic substrates in neurons. Rubicon is a well-established inhibitor of autophagy in all cells.

Effects of low-power laser auriculotherapy on chronic spinal pain: Randomized clinical trial.

Aims And Objectives: To evaluate the effect of laser auriculotherapy on chronic spinal pain. It is a randomized controlled clinical trial.

Methods: Volunteers with chronic spinal pain underwent three evaluations: an initial evaluation, a final evaluation immediately after the last intervention session, and a 15-day follow-up.

Contribution of Autophagy-Lysosomal Pathway in the Exosomal Secretion of Alpha-Synuclein and Its Impact in the Progression of Parkinson's Disease.

Parkinson's disease (PD) is caused by the degeneration of dopaminergic neurons due to an accumulation of intraneuronal abnormal alpha-synuclein (α-syn) protein aggregates. It has been reported that the levels of exosomal α-syn of neuronal origin in plasma correlate significantly with motor dysfunction, highlighting the exosomes containing α-syn as a potential biomarker of PD. In addition, it has been found that the selective autophagy-lysosomal pathway (ALP) contributes to the secretion of misfolded proteins involved in neurodegenerative diseases.

Insulin-like growth factor 2 and autophagy gene expression alteration arise as potential biomarkers in Parkinson's disease.

Insulin-like growth factor 2 (IGF2) and autophagy-related genes have been proposed as biomolecules of interest related to idiopathic Parkinson's disease (PD). The objective of this study was to determine the IGF2 and IGF1 levels in plasma and peripheral blood mononuclear cells (PBMCs) from patients with moderately advanced PD and explore the potential correlation with autophagy-related genes in the same blood samples. IGF1 and IGF2 levels in patients' plasma were measured by ELISA, and the IGF2 expression levels were determined by real-time PCR and Western blot in PBMCs.

DEF8 and Autophagy-Associated Genes Are Altered in Mild Cognitive Impairment, Probable Alzheimer's Disease Patients, and a Transgenic Model of the Disease.

Background: Disturbances in the autophagy/endolysosomal systems are proposed as early signatures of Alzheimer's disease (AD). However, few studies are available concerning autophagy gene expression in AD patients.

Objective: To explore the differential expression of classical genes involved in the autophagy pathway, among them a less characterized one, DEF8 (Differentially expressed in FDCP 8), initially considered a Rubicon family member, in peripheralblood mononuclear cells (PBMCs) from individuals with mild cognitive impairment (MCI) and probable AD (pAD) and correlate the results with the expression of DEF8 in the brain of 5xFAD mice.

Implications of Selective Autophagy Dysfunction for ALS Pathology.

Amyotrophic lateral sclerosis (ALS) is a lethal neurodegenerative disorder that progressively affects motor neurons in the brain and spinal cord. Due to the biological complexity of the disease, its etiology remains unknown. Several cellular mechanisms involved in the neurodegenerative process in ALS have been found, including the loss of RNA and protein homeostasis, as well as mitochondrial dysfunction.

Down syndrome and Alzheimer's disease: common molecular traits beyond the amyloid precursor protein.

Alzheimer's disease (AD) is the most prevalent type of dementia. Down syndrome (DS) is the leading genetic risk factor for Early-Onset AD, prematurely presenting the classic pathological features of the brain with AD. Augmented gene dosage, including the gene, could partially cause this predisposition.

Outside in: Unraveling the Role of Neuroinflammation in the Progression of Parkinson's Disease.

Neuroinflammation is one of the most important processes involved in the pathogenesis of Parkinson's disease (PD). The current concept of neuroinflammation comprises an inflammation process, which occurs in the central nervous system due to molecules released from brain-resident and/or blood-derived immune cells. Furthermore, the evidence of the contribution of systemic delivered molecules to the disease pathogenesis, such as the gut microbiota composition, has been increasing during the last years.

Unraveling the role of motoneuron autophagy in ALS.

In recent years, the role of autophagy in the pathogenesis of most neurodegenerative diseases has transitioned into a limbo of protective or detrimental effects. Genetic evidence indicates that mutations in autophagy-regulatory genes can result in the occurrence of amyotrophic lateral sclerosis (ALS), suggesting a physiological role of the pathway to motoneuron function. However, experimental manipulation of autophagy in ALS models led to conflicting results depending on the intervention strategy and the disease model used.

Disulfide cross-linked multimers of TDP-43 and spinal motoneuron loss in a TDP-43 ALS/FTD mouse model.

Tar DNA binding protein 43 (TDP-43) is the principal component of ubiquitinated protein inclusions present in nervous tissue of most cases of both amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). Previous studies described a TDP-43 transgenic mouse model that develops progressive motor dysfunction in the absence of protein aggregation or significant motoneuron loss, questioning its validity to study ALS. Here we have further characterized the course of the disease in TDP-43 mice using a battery of tests and biochemical approaches.

The Enigmatic Role of C9ORF72 in Autophagy.

Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease characterized by the loss of motor neurons resulting in a progressive and irreversible muscular paralysis. Advances in large-scale genetics and genomics have revealed intronic hexanucleotide repeat expansions in the gene encoding C9ORF72 as a main genetic cause of ALS and frontotemporal dementia (FTD), the second most common cause of early-onset dementia after Alzheimer's disease. Novel insights regarding the underlying pathogenic mechanisms of C9ORF72 seem to suggest a synergy of loss and gain of toxic function during disease.

BAX inhibitor-1 regulates autophagy by controlling the IRE1α branch of the unfolded protein response.

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Pathogenic role of BECN1/Beclin 1 in the development of amyotrophic lateral sclerosis.

Pharmacological activation of autophagy is becoming an attractive strategy to induce the selective degradation of aggregate-prone proteins. Recent evidence also suggests that autophagy impairment may underlie the pathogenesis of several neurodegenerative diseases. Mutations in the gene encoding SOD1 (superoxide disumutase 1) trigger familial amyotrophic lateral sclerosis (ALS), inducing its misfolding and aggregation and the progressive loss of motoneurons.

Functional contribution of the transcription factor ATF4 to the pathogenesis of amyotrophic lateral sclerosis.

Endoplasmic reticulum (ER) stress represents an early pathological event in amyotrophic lateral sclerosis (ALS). ATF4 is a key ER stress transcription factor that plays a role in both adaptation to stress and the activation of apoptosis. Here we investigated the contribution of ATF4 to ALS.

Trehalose delays the progression of amyotrophic lateral sclerosis by enhancing autophagy in motoneurons.

Amyotrophic lateral sclerosis (ALS) is a fatal motoneuron disease with no current effective treatment. Accumulation of abnormal protein inclusions containing SOD1, TARDBP, FUS, among other proteins, is a pathological hallmark of ALS. Autophagy is the major degradation pathway involved in the clearance of damaged organelles and protein aggregates.

Autophagy impairment: a crossroad between neurodegeneration and tauopathies.

Most neurodegenerative diseases involve the accumulation of misfolded proteins in the nervous system. Impairment of protein degradation pathways such as autophagy is emerging as a consistent and transversal pathological phenomenon in neurodegenerative diseases, including Alzheimer's, Huntington's, and Parkinson's disease. Genetic inactivation of autophagy in mice has demonstrated a key role of the pathway in maintaining protein homeostasis in the brain, triggering massive neuronal loss and the accumulation of abnormal protein inclusions.

BAX inhibitor-1 regulates autophagy by controlling the IRE1α branch of the unfolded protein response.

Both autophagy and apoptosis are tightly regulated processes playing a central role in tissue homeostasis. Bax inhibitor 1 (BI-1) is a highly conserved protein with a dual role in apoptosis and endoplasmic reticulum (ER) stress signalling through the regulation of the ER stress sensor inositol requiring kinase 1 α (IRE1α). Here, we describe a novel function of BI-1 in the modulation of autophagy.

Chronic stress and lithium treatments alter hippocampal glutamate uptake and release in the rat and potentiate necrotic cellular death after oxygen and glucose deprivation.

This study was undertaken to evaluate the effects of chronic variate stress and lithium treatment on glutamatergic activity and neuronal vulnerability of rat hippocampus. Male Wistar rats were simultaneously treated with lithium and submitted to a chronic variate stress protocol during 40 days, and afterwards the hippocampal glutamatergic uptake and release, measured in slices and synaptosomes, were evaluated. We observed an increased synaptosomal [(3)H]glutamate uptake and an increase in [(3)H]glutamate stimulated release in hippocampus of lithium-treated rats.

Targeting autophagy in ALS: a complex mission.

Several neurodegenerative diseases share a common neuropathology, primarily featuring the presence of abnormal protein inclusions in the brain containing specific misfolded proteins. Strategies to decrease the load of protein aggregates and oligomers are considered relevant targets for therapeutic intervention. Many studies indicate that macroautophagy is a selective and efficient mechanism for the degradation of misfolded mutant proteins related to neurodegeneration, without affecting the levels of the corresponding wild-type form.

Amyotrophic lateral sclerosis pathogenesis: a journey through the secretory pathway.

Amyotrophic lateral sclerosis (ALS) is the most common adult-onset motoneuron degenerative disease characterized by the selective loss of motoneurons in the spinal ventral horn, most brainstem nuclei, and the cerebral cortex. Although approximately 90% of ALS cases are sporadic (sALS), analyses of familial ALS (fALS)-causative genes have generated relevant insight into molecular events involved in the pathology. Here we overview an emerging concept indicating the occurrence of secretory pathway stress in the disease process.