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BioMed Research International 2020Chemokine CC motif ligand 2 (CCL2) is one of the most recognized proinflammatory chemokines, and the expression of CCL2 in the cerebrospinal fluid of patients infected...
Chemokine CC motif ligand 2 (CCL2) is one of the most recognized proinflammatory chemokines, and the expression of CCL2 in the cerebrospinal fluid of patients infected with HIV-1 is significantly higher than that of healthy people. As such, it is seen as an important cause of HIV-associated neurocognitive disorder (HAND). Our previous investigation has confirmed the pathological role of CCL2 in mediating brain damage leading to cognitive dysfunction. Currently, however, research on therapeutic drugs for the central nervous system targeting CCL2 is very limited. Our present study used brain stereotactic technology to induce cognitive impairment in rats by injecting CCL2 (5 ng) into the bilateral hippocampus. To investigate the protective effect and mechanism of Tanshinone IIA (25, 50, 75 mg/kg/d) on CCL2-induced learning memory and cognitive impairment in rats, we performed the Morris water maze (MWM) and novel object recognition tests (NORT) on the rats. The results showed that Tanshinone IIA significantly alleviated CCL2-induced learning memory and cognitive dysfunction. Further studies on the hippocampal tissue of the rats revealed that Tanshinone IIA treatment significantly increased the activity of SOD and GSH-Px while the level of MDA decreased compared to the model group. Additionally, the relative expression of apoptosis-associated genes caspase-3, caspase-8, and caspase-9 and inflammation-associated genes IL-1 and IL-6 in Tanshinone IIA-treated rats was lower than that in model rats. Finally, we confirmed hippocampal neuron loss and apoptosis by Nissl staining and TdT-mediated dUTP Nick end labeling (TUNEL). Taken together, these data imply that Tanshinone IIA can ameliorate CCL2-induced learning memory and cognitive impairment by impacting oxidative stress, inflammation, and apoptosis. Tanshinone IIA may be a potential therapeutic agent for the treatment of HAND.
Topics: Abietanes; Animals; Apoptosis; Apoptosis Regulatory Proteins; Chemokine CCL2; Cognition; Cognitive Dysfunction; Disease Models, Animal; HIV Infections; Hippocampus; In Situ Nick-End Labeling; Inflammation; Male; Memory; Memory Disorders; Rats; Rats, Sprague-Dawley
PubMed: 32185196
DOI: 10.1155/2020/2702175 -
Dental Traumatology : Official... Dec 2022Delayed treatment of a mandibular fracture can lead to complications. Therefore, early diagnosis is important. The aim of this study was to clarify the specific features...
BACKGROUND/AIMS
Delayed treatment of a mandibular fracture can lead to complications. Therefore, early diagnosis is important. The aim of this study was to clarify the specific features of mandibular fractures in aged patients and the effect of age on possible missed diagnoses.
MATERIAL AND METHODS
Patients aged over 60 years with a recent mandibular fracture were included in the study. The outcome variable was a missed mandibular fracture during the patient's first assessment in the primary health care facility. Predictor variables were age group, categorized as older adults (aged ≥60 and <80 years), elders (aged >80 years), patient's age as a continuous variable and age sub-group divided into decades. Additional predictor variables were the patient's memory disease and injury associated with intracranial injury. Explanatory variables were gender, injury mechanism, type of mandibular facture, combined other facial fracture, edentulous mandible/maxilla/both, surgical treatment of the mandibular fracture, and scene of injury.
RESULTS
Mandibular fractures were missed in 20.0% of the 135 patients during their first healthcare assessment. Significant associations between missed fractures and age group, gender, fracture type, or injury mechanism were not found. By contrast, memory disorder (p = .02) and site of injury (p = .02) were significantly associated with missed fractures. Fractures were missed more frequently in patients who were in hospital or in a nursing home at the time of injury.
CONCLUSIONS
There is an increased risk of undiagnosed mandibular fractures in the aged population. Small injury force accidents may cause fractures in old and fragile individuals. Careful examination is necessary, especially in patients with memory disorder.
Topics: Humans; Middle Aged; Aged; Mandibular Fractures; Mandible; Skull Fractures; Memory Disorders; Retrospective Studies
PubMed: 35950946
DOI: 10.1111/edt.12778 -
Revista de Saude Publica Oct 2018To investigate macroregional variations in cognitive function in a national sample representative of the Brazilian population aged 50 years and older.
OBJECTIVE
To investigate macroregional variations in cognitive function in a national sample representative of the Brazilian population aged 50 years and older.
METHODS
Data from the baseline of the Longitudinal Study of Brazilian Elderly (ELSI-Brazil), collected between 2015 and 2016, were used. Memory was measured by means of a 10-word list and executive function, by semantic verbal fluency, based on the naming of animals. Gender, age, education, and rural or urban residence were potentially confounding.
RESULTS
Among the 9,412 ELSI-Brazil participants, 9,085 were included in the analysis; 53.9% were women and the average age was 63.0 (0.42) years. After adjusting for potential confounding variables, average scores for memory and verbal fluency were lower in the Northeast region and higher in the Midwest and Southeast, respectively. In the South region, higher scores were found for immediate and combined memory. In all regions, older participants and those with lower schooling had worse scores for memory and verbal fluency.
CONCLUSIONS
There are differences in cognitive function among older adults in the different macroregions, independent of age, gender, schooling, and rural or urban residence.
Topics: Aged; Aged, 80 and over; Brazil; Cognition; Educational Status; Female; Humans; Longitudinal Studies; Male; Memory Disorders; Middle Aged; Neuropsychological Tests; Rural Population; Urban Population
PubMed: 30379286
DOI: 10.11606/S1518-8787.2018052000629 -
Acta Neurobiologiae Experimentalis 2021Advanced glycation end products (AGEs) have been reported to cause neurodegeneration, senile plaque formation and spatial learning and memory deficits. There is much...
Advanced glycation end products (AGEs) have been reported to cause neurodegeneration, senile plaque formation and spatial learning and memory deficits. There is much evidence describing the beneficial effects of aminoguanidine (AG) on the central nervous system; AG is able to inhibit the receptor for AGEs and beta-amyloid (Aβ) deposition in the brain, thus preventing cognitive decline and neurodegeneration. In this study, we investigated whether AG protects against ovariectomy-induced neuronal deficits and Aβ deposition in rats. Animals in the ovariectomy group (OVX) group, and those in the OVX+AG group were treated with AG (100 mg/kg/day) for 8 weeks. Learning and memory were evaluated using the electric Y maze. AGE and Aβ biochemical assessments were performed using enzyme-linked immunosorbent assay (ELISA) kits. Furthermore, evaluations of brain amyloid precursor protein 695 (APP) mRNA expression by RT-PCR and AGE expression by immunohistochemistry were carried out. Ovariectomized rats exhibited memory impairment and Aβ production disorder with upregulated APP mRNA and AGE expression levels. AG pretreatment relieved the ovariectomy-induced learning and memory disorder and significantly ameliorated the Aβ production disturbance and AGE generation. Additionally, pathological changes in morphology were also significantly recovered. Our data reveal that AG plays a potentially neuroprotective role against ovariectomy-induced learning and cognitive impairment and Aβ production disorder. Advanced glycation end products (AGEs) have been reported to cause neurodegeneration, senile plaque formation and spatial learning and memory deficits. There is much evidence describing the beneficial effects of aminoguanidine (AG) on the central nervous system; AG is able to inhibit the receptor for AGEs and beta-amyloid (Aβ) deposition in the brain, thus preventing cognitive decline and neurodegeneration. In this study, we investigated whether AG protects against ovariectomy-induced neuronal deficits and Aβ deposition in rats. Animals in the ovariectomy group (OVX) group, and those in the OVX+AG group were treated with AG (100 mg/kg/day) for 8 weeks. Learning and memory were evaluated using the electric Y maze. AGE and Aβ biochemical assessments were performed using enzyme-linked immunosorbent assay (ELISA) kits. Furthermore, evaluations of brain amyloid precursor protein 695 (APP) mRNA expression by RT-PCR and AGE expression by immunohistochemistry were carried out. Ovariectomized rats exhibited memory impairment and Aβ production disorder with upregulated APP mRNA and AGE expression levels. AG pretreatment relieved the ovariectomy-induced learning and memory disorder and significantly ameliorated the Aβ production disturbance and AGE generation. Additionally, pathological changes in morphology were also significantly recovered. Our data reveal that AG plays a potentially neuroprotective role against ovariectomy-induced learning and cognitive impairment and Aβ production disorder.
Topics: Amyloid beta-Peptides; Amyloid beta-Protein Precursor; Animals; Brain; Cognitive Dysfunction; Guanidines; Memory; Memory Disorders; Neurons; Ovariectomy; Rats
PubMed: 33949165
DOI: 10.21307/ane-2021-002 -
Aging Clinical and Experimental Research Aug 2021COVID-19 is erupting globally. Mass quarantine had been implemented all around China which could influence the psychological status of patients with memory disorders and...
BACKGROUND
COVID-19 is erupting globally. Mass quarantine had been implemented all around China which could influence the psychological status of patients with memory disorders and their caregivers.
AIM
To investigate the psychological impact of mass quarantine on patients with memory disorders and their caregivers in China.
METHODS
We completed a cross-sectional study in 787 patients and their caregivers registered from 2010 to 2019 in Memory Clinic, The First Affiliated Hospital of Chongqing Medical University, by telephone interviews. The performance in neuropsychiatric symptoms (NPSs), sleep, nutrition, chronic diseases of patients, and the burden of care, anxiety and depression of caregivers was assessed by six assessment scales (MNA-SF, PSQI, NPI, RSS, PHQ-9 and GAD-7).
RESULTS
Only 68 (8.6%) patients worried about the outbreak of COVID-19. The prevalence of NPSs among all subjects was nearly 60.0%. Approximately 50.0% of the caregivers reported distress. More than 70.0% of patients remained stable in NPSs. However, anxiety, depression, aberrant motor disorder and delusion were exacerbated (22.9%, 18.6%, 17.1% and 16.8%, respectively). Appetite and eating disorder led alleviation rate by 25.8% while disappearing rate of agitation led by 5.8%. 7.5% of caregivers manifested depressive symptoms while 4.9% expressed anxiety symptoms, and 40.8% showed care burden. The coefficients of RSS and PHQ-9, RSS and GAD-7, RSS and NPI-D, PHQ-9 and GAD-7 were 0.7, 0.5, 0.5 and 0.6, respectively (p < 0.01).
CONCLUSION
Changes in NPSs during COVID-19 were observed in some patients with memory disorders and their caregivers, and adherence to medication contributed to the stabilization of NPSs.
Topics: Anxiety; COVID-19; Caregivers; China; Cross-Sectional Studies; Dementia; Humans; Memory Disorders; SARS-CoV-2
PubMed: 34159534
DOI: 10.1007/s40520-021-01911-1 -
Neuropsychology Sep 2023Subtle decline in memory is thought to arise in the preclinical phase of Alzheimer's disease (AD). However, detecting these initial cognitive difficulties...
OBJECTIVE
Subtle decline in memory is thought to arise in the preclinical phase of Alzheimer's disease (AD). However, detecting these initial cognitive difficulties cross-sectionally has been challenging, and the exact nature of the decline is still debated. Accelerated long-term forgetting (ALF) has been recently suggested as one of the earliest and most sensitive indicators of memory dysfunction in subjects at risk of developing AD. The objective of this study was to design and validate the 1-week memory battery (1WMB) for assessing episodic memory and ALF in cognitively unimpaired individuals.
METHOD
The 1WMB is unique in that it assesses multimodal memory and measures recall at both short delay (20 min) and at long term (1 week). Forty-five cognitively unimpaired subjects were assessed with 1WMB and standardized neuropsychological tests. Subjective cognitive decline (SCD), levels of anxiety and depression, and cognitive reserve were also measured.
RESULTS
The tests of 1WMB showed a high internal consistency, and concurrent validity was observed with standard tests of episodic memory and executive functions. The analysis revealed a greater loss of information at 1 week compared to short-term forgetting (20 min). Performance in the 1WMB was affected by age and educational level, but was not associated with levels of anxiety and depression. Unlike standard tests, performance in the 1WMB correlated with measures of SCD.
CONCLUSION
Our findings indicate that the 1WMB has good psychometric properties, and future studies are needed to explore its potential usefulness to assess cognitively unimpaired subjects at increased risk of developing AD. (PsycInfo Database Record (c) 2023 APA, all rights reserved).
Topics: Humans; Memory, Episodic; Neuropsychological Tests; Alzheimer Disease; Mental Recall; Executive Function; Cognitive Dysfunction; Memory Disorders
PubMed: 36729500
DOI: 10.1037/neu0000879 -
Psychogeriatrics : the Official Journal... Jun 2013Dementia with Lewy bodies (DLB) is defined pathologically as neurodegeneration associated with Lewy bodies (LB). LB-related symptoms, including olfactory dysfunction,... (Review)
Review
Dementia with Lewy bodies (DLB) is defined pathologically as neurodegeneration associated with Lewy bodies (LB). LB-related symptoms, including olfactory dysfunction, dysautonomia, and mood and sleep disorders, are increasingly recognized as clinical signs that enable the early detection of DLB, because these symptoms often antedate dementia by years or even decades. It remains unknown if the clinical history of LB-related symptoms is sufficient for the prodromal state of DLB to be suspected in memory clinics. We retrospectively investigated the clinical courses, including olfactory dysfunction, dysautonomia, depression, and rapid eye movement sleep behaviour disorder, of 90 patients with probable DLB. The timing of LB-related symptoms that preceded or followed relative to the onset of memory loss was calculated. LB-related symptoms were present in 79 of 90 patients (87.8%) with probable DLB before or at the time of memory loss onset. These symptoms preceded the onset of memory loss between 1.2 and 9.3 years. We also report on four non-demented patients with a clinical history of LB-related symptoms in our memory clinic. All four patients showed reduced cardiac [(123) I]-metaiodobenzylguanidine levels. Moreover, [(18) F]fluoro-D-glucose positron emission tomography scans revealed glucose hypometabolism in the occipital cortex in two patients. One patient converted to probable DLB with the development of parkinsonism 2 years after major depression was diagnosed. Based on a clinical history of LB-related symptoms, we propose a conceptual framework to identify these symptomatic but non-demented individuals that led us to suspect the underlying pathophysiology of Lewy body disease. Further prospective study is warranted to determine the clinical significance of LB-related symptoms in non-demented patients.
Topics: Cognitive Dysfunction; Dementia; Humans; Lewy Body Disease; Memory Disorders; Positron-Emission Tomography; Prodromal Symptoms; Prospective Studies; Sleep Wake Disorders; Sleep, REM
PubMed: 23909972
DOI: 10.1111/psyg.12005 -
Scientific Reports Mar 2017Sleep disorder is becoming a widespread problem in current society, and is associated with impaired cognition and emotional disorders. Progranulin (PGRN), also known as...
Sleep disorder is becoming a widespread problem in current society, and is associated with impaired cognition and emotional disorders. Progranulin (PGRN), also known as granulin epithelin precursor, promotes neurite outgrowth and cell survival, and is encoded by the GRN gene. It is a tumor necrosis factor α receptor (TNFR) ligand which is implicated in many central nervous system diseases. However, the role PGRN in sleep disorder remains unclear. In the present study, we found that sleep deprivation (S-DEP) impaired the memory and produced thigmotaxis/anxiety-like behaviors in mice. S-DEP increased the levels of TNFα but decreased PGRN levels in the hippocampus. The intracerebroventricular (ICV) injection of PGRN or intraperitoneal injection of TNFα synthesis blocker thalidomide (25 mg/kg), prevented the memory impairment and anxiety behaviors induced by S-DEP. PGRN treatment also restored dendritic spine density in the hippocampus CA1 region and neurogenesis in hippocampus dentate gyrus (DG). These results indicate that an imbalance between TNFα and PGRN contributes to memory impairment and thigmotaxis/anxiety caused by sleep deprivation.
Topics: Animals; Anxiety; Behavior, Animal; Dendritic Spines; Granulins; Hippocampus; Intercellular Signaling Peptides and Proteins; Memory Disorders; Mice; Neurogenesis; Progranulins; Signal Transduction; Sleep Deprivation; Tumor Necrosis Factor-alpha
PubMed: 28300056
DOI: 10.1038/srep43594 -
Dialogues in Clinical Neuroscience Mar 2012Human memory is not a literal reproduction of the past, but instead relies on constructive processes that are sometimes prone to error and distortion. Understanding of... (Review)
Review
Human memory is not a literal reproduction of the past, but instead relies on constructive processes that are sometimes prone to error and distortion. Understanding of constructive memory has accelerated during recent years as a result of research that has linked together its cognitive and neural bases. This article focuses on three aspects of constructive memory that have been the target of recent research: (i) the idea that certain kinds of memory distortions reflect the operation of adaptive cognitive processes that contribute to the efficient functioning of memory; (ii) the role of a constructive memory system in imagining or simulating possible future events; and (iii) differences between true and false memories that have been revealed by functional neuroimaging techniques. The article delineates the theoretical implications of relevant research, and also considers some clinical and applied implications.
Topics: Clinical Trials as Topic; Cognition; Forecasting; Humans; Imagination; Memory; Memory Disorders
PubMed: 22577300
DOI: 10.31887/DCNS.2012.14.1/dschacter -
Neuropsychologia Sep 2016Dissociative experiences, involving altered states of consciousness, have long been understood as a consequence or response to traumatic experiences, where a reduced... (Review)
Review
Dissociative experiences, involving altered states of consciousness, have long been understood as a consequence or response to traumatic experiences, where a reduced level of consciousness may aid in survival during and after a traumatic event. Indeed, the dissociative subtype of post-traumatic stress disorder (PTSD-DS) was added recently to the Diagnostic and Statistical Manual of Mental Disorders, 5th edition (DSM-5). Dissociative symptoms are present across a host of neuropsychiatric conditions, including PTSD, psychotic spectrum illnesses, anxiety and mood disorders. Transdiagnostically, the presence of dissociative symptoms is associated with a greater illness burden and reduced treatment outcomes. Critically, dissociative symptoms are related to impaired performance on measures of attention, executive functioning, memory, and social cognition and may contribute to the widespread cognitive dysfunction observed across psychiatric illnesses. Despite this knowledge, the relation between dissociative symptoms and reduced cognitive function remains poorly understood. Here, we review the evidence linking dissociative symptoms to cognitive dysfunction across neuropsychiatric disorders. In addition, we explore two potential neurobiological mechanisms that may underlie the relation between dissociative symptoms and cognitive dysfunction in trauma-related neuropsychiatric conditions. Specifically, we hypothesize that: 1) functional sensory deafferentation at the level of the thalamus, as observed in the defence cascade model of dissociation, may underlie reduced attention and arousal leading to progressive cognitive dysfunction and; 2) altered functional connectivity between key brain networks implicated in cognitive functioning may represent a critical neurobiological mechanism linking dissociative symptoms and cognitive dysfunction in patients with PTSD-DS and transdiagnostically.
Topics: Cognition Disorders; Dissociative Disorders; Executive Function; Humans; Memory Disorders; Mental Disorders; Military Psychiatry; Social Behavior
PubMed: 27444881
DOI: 10.1016/j.neuropsychologia.2016.07.017