-
Advances in Neurobiology 2021The role of astrocytes in the nervous system pathology was early on embraced by neuroscientists at end of the nineteenth and the beginning of the twentieth century, only...
The role of astrocytes in the nervous system pathology was early on embraced by neuroscientists at end of the nineteenth and the beginning of the twentieth century, only to be pushed aside by neurone-centric dogmas during most of the twentieth century. However, the last decade of the twentieth century and the twenty-first century have brought the astroglial "renaissance", which has put astroglial cells as key players in pathophysiology of most if not all disorders of the nervous system and has regarded astroglia as a fertile ground for therapeutic intervention.Astrocytic contribution to neuropathology can be primary, whereby cell-autonomous changes, such as mutations in gene encoding for glial fibrillary acidic protein, can drive the pathologic progression, in this example, Alexander disease. They can also be secondary, when astrocytes respond to a variety of insults to the nervous tissue. Regardless of their origin, being cell-autonomous or not, changes in astroglia that occur in pathology, that is, astrogliopathology, can be contemporary and arbitrary classified into four forms: (i) reactive astrogliosis, (ii) astrocytic atrophy with loss of function, (iii) pathological remodelling of astrocytes and (iv) astrodegeneration morphologically manifested as clasmatodendrosis. Inevitably, as with any other classification, this classification of astrogliopathology awaits its revision that shall be rooted in new discoveries and concepts.
Topics: Alexander Disease; Astrocytes; Atrophy; Gliosis; Humans
PubMed: 34888830
DOI: 10.1007/978-3-030-77375-5_3 -
International Journal of Environmental... Aug 2023Sarcopenia is the loss of muscle mass and function from aging, inactivity, or disuse. It is a comorbidity to numerous conditions that exacerbates their severity and... (Review)
Review
Sarcopenia is the loss of muscle mass and function from aging, inactivity, or disuse. It is a comorbidity to numerous conditions that exacerbates their severity and adversely impacts activities of daily living. While sarcopenia now receives more attention from the medical community, people with sarcopenia as a comorbidity nevertheless still sometimes receives less attention than other presenting diseases or conditions. Inevitable doctors' visits or hospital stays for those with sarcopenia as a comorbidity have far higher healthcare costs than those without this condition, which imposes a greater financial burden on the medical insurance and healthcare industries. This review offers information and guidance on this topic. Treatments for sarcopenia include dietary, exercise, and pharmacological interventions. Yet, the latter treatment is only recommended in extreme cases as it may evoke numerous side effects and has little support in the scientific literature. Currently, a more holistic approach, with an emphasis on lifestyle modification, to reduce the likelihood of sarcopenia is examined. The current review discusses dietary and exercise interventions to limit the occurrence and severity of sarcopenia. References cited in this review conformed to the Declaration of Helsinki requirements for the use of human research subjects. Most of this review's references (~97%) came from a PubMed search that spanned from 1997 to 2023. Search terms included "sarcopenia" OR "muscle wasting" OR "geriatrics"; OR "ageing"; and AND "diet" OR "exercise". In addition, papers relevant or supportive of the topic as well as those considered seminal were included in the review. Over 96% of the references were peer-reviewed articles.
Topics: Humans; Activities of Daily Living; Diet; Sarcopenia; Aging; Muscular Atrophy
PubMed: 37681791
DOI: 10.3390/ijerph20176652 -
JCI Insight Dec 2022Muscle weakness and wasting are defining features of cancer-induced cachexia. Mitochondrial stress occurs before atrophy in certain muscles, but the possibility of...
Muscle weakness and wasting are defining features of cancer-induced cachexia. Mitochondrial stress occurs before atrophy in certain muscles, but the possibility of heterogeneous responses between muscles and across time remains unclear. Using mice inoculated with Colon-26 cancer, we demonstrate that specific force production was reduced in quadriceps and diaphragm at 2 weeks in the absence of atrophy. At this time, pyruvate-supported mitochondrial respiration was lower in quadriceps while mitochondrial H2O2 emission was elevated in diaphragm. By 4 weeks, atrophy occurred in both muscles, but specific force production increased to control levels in quadriceps such that reductions in absolute force were due entirely to atrophy. Specific force production remained reduced in diaphragm. Mitochondrial respiration increased and H2O2 emission was unchanged in both muscles versus control while mitochondrial creatine sensitivity was reduced in quadriceps. These findings indicate muscle weakness precedes atrophy and is linked to heterogeneous mitochondrial alterations that could involve adaptive responses to metabolic stress. Eventual muscle-specific restorations in specific force and bioenergetics highlight how the effects of cancer on one muscle do not predict the response in another muscle. Exploring heterogeneous responses of muscle to cancer may reveal new mechanisms underlying distinct sensitivities, or resistance, to cancer cachexia.
Topics: Mice; Animals; Cachexia; Muscle, Skeletal; Hydrogen Peroxide; Muscle Weakness; Atrophy; Colonic Neoplasms
PubMed: 36346680
DOI: 10.1172/jci.insight.155147 -
Biomedicine & Pharmacotherapy =... Sep 2021Atrophy is defined as a reduction in cell, organ, or tissue size after reaching their normal mature sizes because of loss of organelles, cytoplasmic compartments, and... (Review)
Review
Atrophy is defined as a reduction in cell, organ, or tissue size after reaching their normal mature sizes because of loss of organelles, cytoplasmic compartments, and proteins. This process is also involved in the pathogenesis of human disorders. Inadequate nourishment, poor circulation, inadequate hormonal support, defects in nerve supply of the tissue, disproportionate induction of apoptosis in the tissue, and absence of exercise are some underlying causes of atrophy. Recently, several non-coding RNAs (ncRNAs) have been identified that regulate atrophy, thus participating in the pathobiology of related disorders such as neurodegenerative/ neuromuscular diseases, age-related muscle atrophy, and cardiac tissue atrophy. In the current review, we have focused on two classes of ncRNAs namely long ncRNAs (lncRNAs) and microRNAs (miRNAs) to unravel their participation in atrophy-associated disorders.
Topics: Animals; Atrophy; Humans; RNA, Long Noncoding
PubMed: 34146849
DOI: 10.1016/j.biopha.2021.111820 -
Medicina (Kaunas, Lithuania) Sep 2019The aim of this review is to provide an overview of genitourinary health in peri- and postmenopause, particularly of vulvovaginal atrophy (VVA), which is part of... (Review)
Review
The aim of this review is to provide an overview of genitourinary health in peri- and postmenopause, particularly of vulvovaginal atrophy (VVA), which is part of genitourinary syndrome (GSM). This condition has a high prevalence among post-menopausal women and negatively affects a woman's quality of life. Epidemiology, signs, symptoms, diagnostic criteria of VVA and target treatments for restoring vaginal health are discussed in light of the most recent literature. Issues related to this condition in menopausal women are under-diagnosed, lack objective diagnostic criteria, and consequently under-treated. Over the years, many treatments have been developed but their long-term effectiveness and safety have yet to be clearly defined. Patients are often dissatisfied and stop treatment, suggesting the need for a more personalized and tailored approach to achieve better compliance and thereby effectiveness. The aim of this paper is to provide an overview of the most recent literature on VVA in order to help the gynecologist in the management of this condition.
Topics: Administration, Intravaginal; Atrophy; Emollients; Female; Hormone Replacement Therapy; Humans; Laser Therapy; Lubricants; Perimenopause; Postmenopause; Vagina; Vaginal Diseases
PubMed: 31547180
DOI: 10.3390/medicina55100615 -
Laboratory Investigation; a Journal of... Aug 2023In multiple sclerosis (MS), demyelination occurs in the cerebral cortex, and cerebral cortex atrophy correlates with clinical disabilities. Treatments are needed in MS...
In multiple sclerosis (MS), demyelination occurs in the cerebral cortex, and cerebral cortex atrophy correlates with clinical disabilities. Treatments are needed in MS to induce remyelination. Pregnancy is protective in MS. Estriol is made by the fetoplacental unit, and maternal serum estriol levels temporally align with fetal myelination. Here, we determined the effect of estriol treatment on the cerebral cortex in the preclinical model of MS, experimental autoimmune encephalomyelitis (EAE). Estriol treatment initiated after disease onset decreased cerebral cortex atrophy. Neuropathology of the cerebral cortex showed increased cholesterol synthesis proteins in oligodendrocytes, more newly formed remyelinating oligodendrocytes, and increased myelin in estriol-treated EAE mice. Estriol treatment also decreased the loss of cortical layer V pyramidal neurons and their apical dendrites and preserved synapses. Together, estriol treatment after EAE onset reduced atrophy and was neuroprotective in the cerebral cortex.
Topics: Pregnancy; Female; Mice; Animals; Neuroprotection; Encephalomyelitis, Autoimmune, Experimental; Multiple Sclerosis; Estriol; Cerebral Cortex; Neurodegenerative Diseases; Atrophy; Mice, Inbred C57BL
PubMed: 37245852
DOI: 10.1016/j.labinv.2023.100189 -
Journal of Osteopathic Medicine Jan 2023
Topics: Humans; Atrophy
PubMed: 35998653
DOI: 10.1515/jom-2022-0147 -
World Journal of Gastroenterology Nov 2022This editorial provides an update of the recent evidence on the endoscopy-based Kyoto classification of gastritis, clarifying the shortcomings of the Kyoto...
This editorial provides an update of the recent evidence on the endoscopy-based Kyoto classification of gastritis, clarifying the shortcomings of the Kyoto classification, and providing prospects for future research, with particular focus on the histological subtypes of gastric cancer (GC) and () infection status. The total Kyoto score is designed to express GC risk on a score ranging from 0 to 8, based on the following five endoscopic findings: Atrophy, intestinal metaplasia (IM), enlarged folds (EF), nodularity, and diffuse redness (DR). The total Kyoto score reflects status as follows: 0, ≥ 2, and ≥ 4 indicate a normal stomach, -infected gastritis, and gastritis at risk for GC, respectively. Regular arrangement of collecting venules (RAC) predicts non-infection; EF, nodularity, and DR predict current infection; map-like redness (MLR) predicts past infection; and atrophy and IM predict current or past infection. Atrophy, IM, and EF all increase the incidence of -infected GC. MLR is a specific risk factor for -eradicated GC, while RAC results in less GC. Diffuse-type GC can be induced by active inflammation, which presents as EF, nodularity, and atrophy on endoscopy, as well as neutrophil and mononuclear cell infiltration on histology. In contrast, intestinal-type GC develops atrophy and IM, and is consistent between endoscopy and histology. However, this GC risk-scoring design needs to be improved.
Topics: Humans; Atrophy
PubMed: 36483157
DOI: 10.3748/wjg.v28.i43.6078 -
Tomography (Ann Arbor, Mich.) Feb 2022MRI shows the three archetypal patterns of CNS volume loss underlying progressive ataxias in vivo, namely spinal atrophy (SA), cortical cerebellar atrophy (CCA) and... (Review)
Review
MRI shows the three archetypal patterns of CNS volume loss underlying progressive ataxias in vivo, namely spinal atrophy (SA), cortical cerebellar atrophy (CCA) and olivopontocerebellar atrophy (OPCA). The MRI-based CNS atrophy pattern was reviewed in 128 progressive ataxias. A CNS atrophy pattern was identified in 91 conditions: SA in Friedreich's ataxia, CCA in 5 acquired and 72 (24 dominant, 47 recessive,1 X-linked) inherited ataxias, OPCA in Multi-System Atrophy and 12 (9 dominant, 2 recessive,1 X-linked) inherited ataxias. The MRI-based CNS atrophy pattern may be useful for genetic assessment, identification of shared cellular targets, repurposing therapies or the enlargement of drug indications in progressive ataxias.
Topics: Ataxia; Atrophy; Cerebellar Ataxia; Humans; Magnetic Resonance Imaging; Spinocerebellar Degenerations
PubMed: 35202200
DOI: 10.3390/tomography8010035 -
Cortex; a Journal Devoted To the Study... Aug 2023In his epoch-making monograph, Wernicke (1874) claimed that atrophy of the brain cannot cause aphasia. Refuting this claim, Pick (1892, 1898, 1901, 1904a) documented in... (Review)
Review
In his epoch-making monograph, Wernicke (1874) claimed that atrophy of the brain cannot cause aphasia. Refuting this claim, Pick (1892, 1898, 1901, 1904a) documented in increasing detail several cases of aphasia with circumscribed atrophy of the left temporal lobe, frontal lobe, or both, which persuaded Wernicke (1906). To explain why the atrophy is circumscribed and leads to focal symptoms, Pick (1908a) advanced a functional network account. Behavioral, neuroanatomical, and histopathological studies by Dejerine and Sérieux, Fischer, Alzheimer, Altman, Gans, Onari and Spatz, and Stertz further illuminated the clinical syndromes, the exact spatial distributions of the atrophy, the underlying disease, and its laminar specificity. Unaware of these seminal studies, research from the 1970s until now has independently rediscovered all key findings, and also supports Pick's forgotten functional account of the distribution of atrophy and the focal symptoms. His frontal and temporal forms of aphasia foreshadowed what are now called the nonfluent/agrammatic and semantic variants of primary progressive aphasia. Moreover, aphasic symptoms may occur with frontal degeneration (what used to be called "Pick's disease") that yields personality changes and behavioral disturbances, now called the behavioral variant of frontotemporal dementia.
Topics: Humans; Pick Disease of the Brain; Atrophy; Frontotemporal Dementia; Aphasia; Brain; Aphasia, Primary Progressive
PubMed: 37276800
DOI: 10.1016/j.cortex.2023.05.004