The impact of SARS-CoV-2 in dementia across Latin America: A call for an urgent regional plan and coordinated response.

The SARS-CoV-2 global pandemic will disproportionately impact countries with weak economies and vulnerable populations including people with dementia. Latin American and Caribbean countries (LACs) are burdened with unstable economic development, fragile health systems, massive economic disparities, and a high prevalence of dementia. Here, we underscore the selective impact of SARS-CoV-2 on dementia among LACs, the specific strain on health systems devoted to dementia, and the subsequent effect of increasing inequalities among those with dementia in the region.

GERO Cohort Protocol, Chile, 2017-2022: Community-based Cohort of Functional Decline in Subjective Cognitive Complaint elderly.

Background: With the global population aging and life expectancy increasing, dementia has turned a priority in the health care system. In Chile, dementia is one of the most important causes of disability in the elderly and the most rapidly growing cause of death in the last 20 years. Cognitive complaint is considered a predictor for cognitive and functional decline, incident mild cognitive impairment, and incident dementia.

Idiopathic inflammatory myopathy human derived cells retain their ability to increase mitochondrial function.

Idiopathic Inflammatory Myopathies (IIMs) have been studied within the framework of autoimmune diseases where skeletal muscle appears to have a passive role in the illness. However, persiting weakness even after resolving inflammation raises questions about the role that skeletal muscle plays by itself in these diseases. "Non-immune mediated" hypotheses have arisen to consider inner skeletal muscle cell processes as trigger factors in the clinical manifestations of IIMs.

Axonal Degeneration in AD: The Contribution of Aβ and Tau.

Alzheimer's disease (AD) represents the most common age-related neurodegenerative disorder, affecting around 35 million people worldwide. Despite enormous efforts dedicated to AD research over decades, there is still no cure for the disease. Misfolding and accumulation of Aβ and tau proteins in the brain constitute a defining signature of AD neuropathology, and mounting evidence has documented a link between aggregation of these proteins and neuronal dysfunction.

Systematic Review of the Diagnostic Validity of Brief Cognitive Screenings for Early Dementia Detection in Spanish-Speaking Adults in Latin America.

The aim of this study was to evaluate the validity of brief cognitive screening (BCS) tools designed to diagnose mild cognitive impairment (MCI) or dementia in Spanish-speaking individuals over the age of 50 years from Latin America (LA). A systematic search of titles and abstracts in Medline, Biomed Central, Embase, Scopus, Scirus, PsycINFO, LILACS, and SciELO was conducted. Inclusion criteria were papers written in English or Spanish involving samples from Spanish-speaking Latin American individuals published until 2018.

The power of knowledge about dementia in Latin America across health professionals working on aging.

Introduction: Expert knowledge is critical to fight dementia in inequitable regions like Latin American and Caribbean countries (LACs). However, the opinions of aging experts on public policies' accessibility and transmission, stigma, diagnostic manuals, data-sharing platforms, and use of behavioral insights (BIs) are not well known.

Methods: We investigated opinions among health professionals working on aging in LACs (N = 3365) with regression models including expertise-related information (public policies, BI), individual differences (work, age, academic degree), and location.

The Mitochondrial Unfolded Protein Response: A Hinge Between Healthy and Pathological Aging.

Aging is the time-dependent functional decline that increases the vulnerability to different forms of stress, constituting the major risk factor for the development of neurodegenerative diseases. Dysfunctional mitochondria significantly contribute to aging phenotypes, accumulating particularly in post-mitotic cells, including neurons. To cope with deleterious effects, mitochondria feature different mechanisms for quality control.

Fine-Tuning the TGFβ Signaling Pathway by SARA During Neuronal Development.

Neural development is a complex process that involves critical events, including cytoskeleton dynamics and selective trafficking of proteins to defined cellular destinations. In this regard, Smad Anchor for Receptor Activation (SARA) is an early endosome resident protein, where perform trafficking- associated functions. In addition, SARA is also involved in cell signaling, including the TGFβ-dependent pathway.

Inside minds, beneath diseases: social cognition in amyotrophic lateral sclerosis-frontotemporal spectrum disorder.

Objective: To compare social cognition performance between patients with amyotrophic lateral sclerosis (ALS) and those patients with behavioural variant frontotemporal dementia (bvFTD).

Methods: We included 21 participants with ALS, 20 with bvFTD and 21 healthy controls who underwent a comprehensive cognitive battery, including the short version of the Social Cognition and Emotional Assessment (Mini-SEA), which comprises the test and Facial Emotion Recognition Test (FERT); Mini-Mental State Examination; Frontal Assessment Battery; lexical fluency (F-A-S), category fluency (animals/minute), digit span (direct and backwards) tests and the Hayling test. A post hoc analysis was conducted with the patients with ALS divided into two subgroups: patients without cognitive impairment (ALScn; n=13) and patients with cognitive impairment (ALSci; n=8).

Effects of spatial working memory in balance during dual tasking in traumatic brain injury and healthy controls.

The aim of this research was to assess cognitive-motor interactions though dual tasks of working memory in patients with traumatic brain injury (TBI) and control subjects. : Twenty patients with chronic TBI with good functional level and 19 matched healthy controls performed dual working memory tasks (1-back numeric and 1-back spatial (S)) while sitting, standing, and walking. The center of pressure (COP) displacement amplitude, cadence, and error percentage (PER) were recorded as dependent variables.

Neurological soft signs (NSS) and cognitive deficits in HIV associated neurocognitive disorder.

Neurological soft signs (NSS) are frequently found in severe mental disorders, such as Alzheimer's disease, schizophrenia or HIV associated neurocognitive disorder (HAND) which includes asymptomatic neurocognitive impairment (ANI), mild neurocognitive disorder (MND) and HIV-associated dementia. To characterize NSS in patients with HIV we examined them with respect to neuropsychological deficits typically found in the disorder. 67 HIV + patients without a history of head trauma, opportunistic infections, severe psychiatric disorders or acute confounding comorbidities of the Central nervous system (CNS) were recruited.

Concerted Action of AMPK and Sirtuin-1 Induces Mitochondrial Fragmentation Upon Inhibition of Ca Transfer to Mitochondria.

Mitochondria are highly dynamic organelles constantly undergoing fusion and fission. Ca regulates many aspects of mitochondrial physiology by modulating the activity of several mitochondrial proteins. We previously showed that inhibition of constitutive IP3R-mediated Ca transfer to the mitochondria leads to a metabolic cellular stress and eventually cell death.

Experiential Neurorehabilitation: A Neurological Therapy Based on the Enactive Paradigm.

With the arrival of the cognitive paradigm during the latter half of the last century, the theoretical and scientific bases of neurorehabilitation have been linked to the knowledge developed in cognitive neuropsychology and cognitive neuroscience. Although the knowledge generated by these disciplines has made relevant contributions to neurological therapy, their theoretical premises may create limitations in therapeutic processes. The present manuscript has two main objectives: first, to explicitly set forth the theoretical bases of cognitive neurorehabilitation and critically analyze the repercussions that these premises have produced in clinical practice; and second, to propose the enactive paradigm to reinterpret perspectives on people with brain damage and their therapy (assessment and treatment).

Redox modifications in synaptic components as biomarkers of cognitive status, in brain aging and disease.

Aging is a natural process that includes several changes that gradually make organisms degenerate and die. Harman's theory proposes that aging is a consequence of the progressive accumulation of oxidative modifications mediated by reactive oxygen/nitrogen species, which plays an essential role in the development and progression of many neurodegenerative diseases. This review will focus on how abnormal redox modifications induced by age impair the functionality of neuronal redox-sensitive proteins involved in axonal elongation and guidance, synaptic plasticity, and intercellular communication.

Schwann cell reprogramming into repair cells increases miRNA-21 expression in exosomes promoting axonal growth.

Functional recovery after peripheral nerve damage is dependent on the reprogramming of differentiated Schwann cells (dSCs) into repair Schwann cells (rSCs), which promotes axonal regeneration and tissue homeostasis. Transition into a repair phenotype requires expression of c-Jun and Sox2, which transcriptionally mediates inhibition of the dSC program of myelination and activates a non-cell-autonomous repair program, characterized by the secretion of neuronal survival and regenerative molecules, formation of a cellular scaffold to guide regenerating axons and activation of an innate immune response. Moreover, rSCs release exosomes that are internalized by peripheral neurons, promoting axonal regeneration.

The necroptosis pathway and its role in age-related neurodegenerative diseases: will it open up new therapeutic avenues in the next decade?

Introduction: Necroptosis is a programmed form of necrotic cell death. Growing evidence demonstrates that necroptosis contributes to cell demise in different pathological conditions including age-dependent neurodegenerative diseases (NDs). These findings open new avenues for understanding the mechanisms of neuronal loss in NDs, which might eventually translate into novel therapeutic interventions.

Optimising adjacent membrane segmentation and parameterisation in multicellular aggregates by piecewise active contours.

In fluorescence microscopy imaging, the segmentation of adjacent cell membranes within cell aggregates, multicellular samples, tissue, organs, or whole organisms remains a challenging task. The lipid bilayer is a very thin membrane when compared to the wavelength of photons in the visual spectra. Fluorescent molecules or proteins used for labelling membranes provide a limited signal intensity, and light scattering in combination with sample dynamics during in vivo imaging lead to poor or ambivalent signal patterns that hinder precise localisation of the membrane sheets.

Correction: The necroptosis machinery mediates axonal degeneration in a model of Parkinson disease.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

SK channel activation potentiates auranofin-induced cell death in glio- and neuroblastoma cells.

Brain tumours are among the deadliest tumours being highly resistant to currently available therapies. The proliferative behaviour of gliomas is strongly influenced by ion channel activity. Small-conductance calcium-activated potassium (SK/K) channels are a family of ion channels that are associated with cell proliferation and cell survival.

The necroptosis machinery mediates axonal degeneration in a model of Parkinson disease.

Parkinson's disease (PD) is the second most common neurodegenerative condition, characterized by motor impairment due to the progressive degeneration of dopaminergic neurons in the substantia nigra and depletion of dopamine release in the striatum. Accumulating evidence suggest that degeneration of axons is an early event in the disease, involving destruction programs that are independent of the survival of the cell soma. Necroptosis, a programmed cell death process, is emerging as a mediator of neuronal loss in models of neurodegenerative diseases.

Recommendations for the Nonpharmacological Treatment of Apathy in Brain Disorders.

Apathy is a common neuropsychiatric syndrome observed across many neurocognitive and psychiatric disorders. Although there are currently no definitive standard therapies for the treatment of apathy, nonpharmacological treatment (NPT) is often considered to be at the forefront of clinical management. However, guidelines on how to select, prescribe, and administer NPT in clinical practice are lacking.

Decoding the Role of Platelets and Related MicroRNAs in Aging and Neurodegenerative Disorders.

Platelets are anucleate cells that circulate in blood and are essential components of the hemostatic system. During aging, platelet numbers decrease and their aggregation capacity is reduced. Platelet dysfunctions associated with aging can be linked to molecular alterations affecting several cellular systems that include cytoskeleton rearrangements, signal transduction, vesicular trafficking, and protein degradation.

Complex I and II are required for normal mitochondrial Ca homeostasis.

Cytosolic calcium (Ca) entry into mitochondria is facilitated by the mitochondrial membrane potential (ΔΨm), an electrochemical gradient generated by the electron transport chain (ETC). Is has been assumed that as long as mutations that affect the ETC do not affect the ΔΨm, the mitochondrial Ca (Ca) homeostasis remains normal. We show that knockdown of NDUFAF3 and SDHB reduce ETC activity altering Ca efflux and influx rates while ΔΨm remains intact.

Publisher Correction: Non-canonical function of IRE1α determines mitochondria-associated endoplasmic reticulum composition to control calcium transfer and bioenergetics.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.