Anxiety, depression, and memory loss in Chagas disease: a puzzle far beyond neuroinflammation to be unpicked and solved*

Mental disorders such as anxiety, depression, and memory loss have been described in patients with chronic Chagas disease (CD), a neglected tropical disease caused by the protozoan parasite Trypanosoma cruzi. Social, psychological, and biological stressors may take part in these processes. There is a consensus on the recognition of an acute nervous form of CD. In chronic CD patients, a neurological form is associated with immunosuppression and neurobehavioural changes as sequelae of stroke. The chronic nervous form of CD has been refuted, based on the absence of histopathological lesions and neuroinflammation; however, computed tomography shows brain atrophy. Overall, in preclinical models of chronic T. cruzi infection in the absence of neuroinflammation, behavioural disorders such as anxiety and depression, and memory loss are related to brain atrophy, parasite persistence, oxidative stress, and cytokine production in the central nervous system. Interferon-gamma (IFNγ)-bearing microglial cells are colocalised with astrocytes carrying T. cruzi amastigote forms. In vitro studies suggest that IFNγ fuels astrocyte infection by T. cruzi and implicate IFNγ-stimulated infected astrocytes as sources of TNF and nitric oxide, which may also contribute to parasite persistence in the brain tissue and promote behavioural and neurocognitive changes. Preclinical trials in chronically infected mice targeting the TNF pathway or the parasite opened paths for therapeutic approaches with a beneficial impact on depression and memory loss. Despite the path taken, replicating aspects of the chronic CD and testing therapeutic schemes in preclinical models, these findings may get lost in translation as the chronic nervous form of CD does not fulfil biomedical model requirements, as the presence of neuroinflammation, to be recognised. It is hoped that brain atrophy and behavioural and neurocognitive changes are sufficient traits to bring the attention of researchers to study the biological and molecular basis of the central nervous system commitment in chronic CD.

O que é ser uma pessoa idosa que apresenta queixas de memória: a percepção de mulheres atendidas em um Centro de Reabilitação Física / What it is like to be an older person with memory complaints: the perception of women seen at a Physical Rehabilitation Center

Resumo Objetivo Conhecer e compreender o que é ser uma pessoa idosa que apresenta queixas de memória, por meio do olhar de mulheres atendidas em um Centro de Reabilitação Física. Método Estudo descritivo exploratório de caráter qualitativo com população composta por idosas acima de 60 anos que apresentavam alteração da função cognitiva, verificada por meio do instrumento Miniexame do Estado Mental (MEEM) e queixas subjetivas de memória. Foi aplicado um questionário para a caracterização das participantes e realizada uma entrevista semiestruturada áudio gravada baseada em uma pergunta orientadora. As entrevistas transcritas na íntegra foram analisadas com a Análise do Conteúdo de Bardin. Resultados As 19 participantes apresentavam idade entre 62 e 84 anos, com média de 72,37 (±6,72) anos. Por meio da leitura das falas relacionadas as respostas da pergunta orientadora e análise, foi possível identificar duas categorias: (1) sentimentos que as idosas vivenciam devido a queixa de memória; (2) situações da vida diária que são afetadas pela queixa de memória. Conclusão Ser uma idosa que apresenta queixas de memória se mostra como algo difícil, promove diversas mudanças no cotidiano, altera situações que costumavam ser comuns, sendo necessárias readaptações tanto da idosa que sofre com a dificuldade de memória, quanto para os indivíduos que estão a sua volta.

Abstract Objective To understand what it is like to be an older person with memory complaints from the perspective of women seen at a Physical Rehabilitation Center. Method A qualitative exploratory descriptive study was conducted involving a population of older women aged >60 years who had impaired cognitive function, as measured by the Mini-Mental State Examination (MMSE), and subjective memory complaints was carried out. A questionnaire was applied to characterize the participants and an audio-recorded semi-structured interview based on a guiding question was conducted. The transcribed interviews were analyzed using Bardin's Content Analysis. Results The age of the 19 participants ranged from 62 to 84 years, with mean of 72.37 (±6.72) years. Reading and analysis of the discourse produced in response to the guiding question revealed two categories: (1) feelings the older women experienced due to memory complaints; (2) daily life situations affected by memory complaints. Conclusion Being an older woman with memory complaints was reported as challenging, promoting changes in daily life, impacting situations that used to be routine, and requiring readjustments both for the older individual with memory impairment and those around them.

Is the use of high-intensity atorvastatin associated with memory impairment?

High-intensity statins are the cornerstone of medical management in Acute Coronary Syndromes (ACS). However, their effect on neurocognition are less clear. In this prospective observational study, we gave guideline-directed high-intensity atorvastatin 40 mg to middle-aged statin-naïve ACS patients. Memory assessments were performed before and 6 months after statin therapy using 2 validated scales-the PostGraduate Institute Memory Scale (PGI-MS), and the Logical Memory Passage Test (LMPT). There was no significant difference in the mean PGI-MS test scores (baseline 75.4 ± 7.9, 6months 76.5 ± 8.2;p ¼ 0.26) or the overall composite scores (baseline 32.02 ± 3.2, 6months 32.8 ± 3.1; p ¼ 0.20), after 6 months of statin use. There was a small improvement in immediate recall (baseline score 8.5 ± 2.5, 6 months 9.04 ± 1.8; p ¼ 0.05), and delayed recall (baseline 6.1 ± 2.6, 6 months 6.9 ± 1.9, p ¼ 0.002). High-intensity atorvastatin use did not affect memory at 6 months among statin-naïve middle-aged patients with ACS.

Amnesia en el embarazo / Amnesia in Pregnancy

La memoria es la capacidad para aprender, organizar y fijar eventos de nuestro pasado y se encuentra íntimamente ligado a la función de la atención. Es capaz de guardar datos a través de mecanismos ultra complejos que se desarrollan en tres etapas: codificación, almacenamiento y evocación. La presencia de la amnesia impide que esta capacidad se desarrolle adecuadamente. La amnesia ocurre cuando se comprueba que alguien ha perdido o tiene debilitada la memoria. Hay varias causas de pérdida de la memoria, como ha sido señalado, por ejemplo, en la etapa del climaterio y la menopausia donde este aspecto es considerado para clasificar la intensidad del síndrome climatérico que se presenta con frecuencia en esta etapa. La persona que sufre este trastorno no es capaz de almacenar ni de recuperar información recibida con anticipación, ya sea por motivos orgánicos o funcionales. La amnesia (del griego ἀμνησία amnesia, olvido) es la pérdida parcial o completa de la memoria. Sus causas son orgánicas o funcionales. Muchas mujeres, cuando se encuentran embarazadas experimentan una pérdida parcial de memoria a corto plazo conocida como amnesia del embarazo, mumnecia, o lo que los anglosajones suelen llamar placenta's brain (cerebro de placenta). Durante el embarazo, las fluctuaciones hormonales que experimenta la mujer producen cambios en la actividad cerebral, provocando una pérdida parcial de memoria a corto plazo. Sobre este aspecto abordaremos el estado actual que hay sobre este tema(AU)

Memory is the capacity to learn, organize and fix events of our past and is intimately linked to the function of attention. It is capable of saving data through ultra-complex mechanisms that are developed in three stages: coding, storage and evocation. The presence of amnesia prevents this ability from developing properly. Amnesia occurs when it is proven that someone has lost or has weakened memory. There are several causes of memory loss, as has been pointed out, for example, in the climacteric stage and menopause where this aspect is considered to classify the intensity of the climacteric syndrome that frequently occurs in this stage. The person suffering from this disorder is not able to store or retrieve information received in advance, for organic or functional reasons. Amnesia (from Greek ἀμνησία amnesia, forgetfulness) is the partial or complete loss of memory. Many pregnant women experience a partial loss of short-term memory known as pregnancy amnesia, mumnecia, or placenta's brain as the Anglo-Saxons usually call it. During pregnancy, the hormonal fluctuations experienced by women produce changes in brain activity, causing partial loss of short-term memory. On this aspect, we will address the status on this topic(AU)

Inhibition of Rac1-dependent forgetting alleviates memory deficits in animal models of Alzheimer's disease

Accelerated forgetting has been identified as a feature of Alzheimer's disease (AD), but the therapeutic efficacy of the manipulation of biological mechanisms of forgetting has not been assessed in AD animal models. Ras-related C3 botulinum toxin substrate 1 (Rac1), a small GTPase, has been shown to regulate active forgetting in Drosophila and mice. Here, we showed that Rac1 activity is aberrantly elevated in the hippocampal tissues of AD patients and AD animal models. Moreover, amyloid-beta 42 could induce Rac1 activation in cultured cells. The elevation of Rac1 activity not only accelerated 6-hour spatial memory decay in 3-month-old APP/PS1 mice, but also significantly contributed to severe memory loss in aged APP/PS1 mice. A similar age-dependent Rac1 activity-based memory loss was also observed in an AD fly model. Moreover, inhibition of Rac1 activity could ameliorate cognitive defects and synaptic plasticity in AD animal models. Finally, two novel compounds, identified through behavioral screening of a randomly selected pool of brain permeable small molecules for their positive effect in rescuing memory loss in both fly and mouse models, were found to be capable of inhibiting Rac1 activity. Thus, multiple lines of evidence corroborate in supporting the idea that inhibition of Rac1 activity is effective for treating AD-related memory loss.

Una complicación quirúrgica escasamente sospechada: la disfunción cognitiva postoperatoria / A poorly suspected surgical complication: postoperative cognitive dysfunction

Numerosas enfermedades requieren como tratamiento una cirugía, ya sea de emergencia o electiva. Las cirugías pueden tener diversas complicaciones; sin embargo no se consideran las posibles alteraciones cognitivas postoperatorias: delirio del despertar anestésico, delirio postoperatorio y disfunción cognitiva postoperatoria (DCPO). La DCPO es un síndrome clínico caracterizado por alteraciones en la memoria, concentración, atención, comprensión del lenguaje e integración social posterior al uso de anestesia y cirugía que persiste después de tres meses; aunque algunos reportes consideran que no sería una entidad clínica individual. Su incidencia varía del 5,1 al 52,5% dependiendo de la población estudiada, tipo de cirugía, tiempo de la evaluación desde la cirugía y batería neuropsicológica empleada. Los factores de riesgo para DCPO son: edad avanzada, deterioro cognitivo previo, gravedad de enfermedades coexistentes, severidad de la cirugía, duración y tipo de la anestesia, ocurrencia de complicaciones y nivel educativo; siendo imprescindible la realización de una evaluación neuropsicológica antes y después de la cirugía para su diagnóstico. Los mecanismos etiopatogénicos propuestos son: la edad, cambios en la perfusión cerebral, disturbios del sueño, inflamación, efectos de los agentes anestésicos, y fundamentalmente la neuroinflamación. La DCPO es una entidad frecuente y escasamente sospechada, aunque su diagnóstico es controversial. Se sugiere que los pacientes que serán sometidos a cirugías electivas mayores, en especial las cardiacas y cerebrales, sean sometidos a evaluación neuropsicológica previa y a los 3 meses, así como a monitoreo electroencefalográfico intraoperatorio para disminuir la incidencia de DCPO.

Many diseases require surgery as a treatment, either emergency or elective. Surgeries can have various complications; However, the possible postoperative cognitive alterations are not considered: delirium of anesthetic awakening, postoperative delirium and postoperative cognitive dysfunction (PCDP). DCPO is a clinical syndrome characterized by alterations in memory, concentration, attention, understanding of language and social integration after the use of anesthesia and surgery that persists after three months; although some reports consider that it would not be an individual clinical entity. Its incidence varies from 5.1 to 52.5% depending on the population studied, type of surgery, time of evaluation from surgery and neuropsychological battery used. The risk factors for DCPO are: advanced age, previous cognitive impairment, severity of coexisting diseases, severity of the surgery, duration and type of anesthesia, occurrence of complications and educational level; It is essential to carry out a neuropsychological evaluation before and after the surgery for its diagnosis. The proposed etiopathogenic mechanisms are: age, changes in cerebral perfusion, sleep disturbances, inflammation, effects of anesthetic agents, and fundamentally neuroinflammation. The DCPO is a frequent and rarely suspected entity, although its diagnosis is controversial. It is suggested that patients who will undergo major elective surgeries, especially cardiac and cerebral surgeries, undergo previous neuropsychological evaluation at 3 months, and intraoperative electroencephalographic monitoring to reduce the incidence of DCPO.

Protective effects of cultured and fermented ginseng extracts against scopolamine-induced memory loss in a mouse model / 한국실험동물학회지

This study was performed to investigate the effect of a concentrate of fermented wild ginseng root culture (HLJG0701) on memory improvement in the scopolamine (SPL)-induced memory-deficient mouse model. Eight-week-old male ICR mice were used to evaluate the protective effect of HLJG0701 against the SPL-induced memory loss animal model. The Morris water maze test, which measures hippocampus-dependent learning ability, and the Y-maze test, a short-term memory assessment test, were performed and related markers were analyzed. HLJG0701-treated groups displayed significantly reduced acetylcholinesterase activity and increased acetylcholine level compared with the SPL-administered group (SPL-G) (P < 0.05). In the Y-maze test, the spontaneous alternation in al HLJG0711-treated groups was significantly increased compared with that in SPL-G (P < 0.05). In the Morris water maze test, the escape latency and time spent in the target quadrant in all HLJG0701-treated groups were significantly decreased and increased, respectively, compared with those in SPL-G (P < 0.05). In addition, the brain-derived neurotrophic factor level in groups treated with HLJG0701 300 and 600 mg/kg body weight was significantly increased compared with that in SPL-G (P < 0.05). These results suggest that the HLJG0701 may protect against memory loss by inhibiting acetylcholinesterase activity and preventing acetylcholine deficiency.

Neuromyelitis Optica Spectrum Disorder Presented with Acute Memory Loss

Neuromyelitis optica spectrum disorder (NMOSD) can present with various symptoms including optic neuritis, transverse myelitis, and area postrema syndrome. However, acute memory loss is an uncommon clinical presentation of NMOSD. We report a patient with NMO-IgG-antibody-positive NMOSD presenting with only acute memory loss, which suggested the presence of bilateral thalamic lesions. This case indicates that NMOSD needs to be considered in the differential diagnosis of acute memory loss.

Memoria autobiográfica en epilepsia del lóbulo temporal / Autobiographical memory in temporal lobe epilepsy

La epilepsia del lóbulo temporal (ELT) es un tipo de epilepsia focal que se caracteriza por crisis parciales complejas y secundariamente generalizadas; es una enfermedad de difícil control, es decir que no responde adecuadamente al manejo farmacológico. Otra característica es su comorbilidad con trastornos cognitivos secundarios a la frecuencia e intensidad de las crisis epilépticas, afectándose especialmente los procesos mnésicos. Es probable que el paciente con ELT tenga dificultades en la memoria autobiográfica (MA); sin embargo, la evaluación neuropsicológica que se realiza en este tipo de epilepsia, no refleja las quejas que el paciente refiere acerca de su MA, aspecto que altera su calidad de vida. En el presente artículo se exponen los modelos explicativos de la MA así como los métodos de evaluación más usados para este tipo de memoria y, finalmente, se revisan investigaciones acerca de la MA en pacientes con ELT.

Temporal lobe epilepsy (TLE) is a type of focal epilepsy that is mainly characterized by complex secondarily generated seizures. It is a difficult illness to control because it doesn't respond to pharmacological treatment. Another feature of this type of epilepsy is its comorbidity with cognitive disorders that mainly affect memory and depend on the frequency and intensity of seizures. Patients with TLE normally have problems with autobiographical memory (AM), especially in cases where the etiology is hippocampal sclerosis (HS). However, neuropsychological evaluations of this type of epilepsy do not reflect patient complaints about their autobiographical memory, a factor which affects quality of life. In this paper we present the explanatory models of RAM, set out the most common methods used to assess it, and finally research on AM for patients with TLE is revised.

Amnesia retrógrada aislada: descripción clínica y neuroimágenesde un caso / Isolated retrograde amnesia: clinical description and neuroimages of a case

La amnesia retrógrada aislada es un déficit neuropsicológico poco común y sus características clínicas, etiológicas,imagenológicas y de recuperación han sido poco documentadas. El presente artículo reporta el casoclínico de una paciente de 28 años de edad, residente en Medellín, Colombia, quien posterior a un secuestro,sufre pérdida de la memoria remota. Se le practicó una evaluación neuropsicológica, además se le realizaronestudios de neuroimagen estructural y funcional, con el fin de caracterizar un posible daño neurológico...

Rehabilitación neuropsicológica en un caso de amnesia retrógrada aislada / Neuropsychological rehabilitation in an isolated case of retrograde amnesia

La amnesia retrógrada aislada es un déficit neuropsicológico poco común y el empleo de terapia de rehabilitación neuropsicológica no ha sido estudiado ni planteado para estos pacientes. El presente artículo documenta el caso clínico de CE, una paciente de 28 años de edad, residente en Medellín, Colombia, quien posterior a un secuestro, sufre pérdida de la memoria remota. Se le practicó una evaluación neuropsicológica, y estudios de neuroimagen estructural. Posteriormente, se propuso e implementó un plan de rehabilitación neuropsicológica enfocado en la recuperación de la memoria semántica. Al terminar la intervención se encontró mejoría a nivel cognitivo y funcional, con incremento significativo en las habilidades mnésicas y neurolingüísticas, en la comprensión de su entorno y el desempeño en las actividades cotidianas.

Isolated retrograde amnesia is a rare neuropsychological deficit and neuropsychological rehabilitation therapy has not been studied or proposed for these patients. This article documents the case of CE, a 28-year-old female patient, resident in Medellin, Colombia, who suffers remote memory loss after being kidnapped. Neuropsychological assessment and structural neuroimaging studies was performed. Then, a neuropsychological rehabilitation plan focused on semantic memory retrieval was planned and implemented. After the intervention, cognitive and functional improvement was found, with significant increase in mnemonic and neurolinguistic skills, also in understanding of her environment and her performance in daily activities.

Acetylcholinesterase and butyrylcholinesterase inhibitory activity of some selected Nigerian medicinal plants / Atividade inibitória da acetilcolinesterase e butirilcolinesterase de algumas plantas medicinais da Nigéria

Plants have been found to be useful as memory enhansers as well as antiaging. Twenty two of such plants from sixteen families were investigated for their acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) inhibitory activities using the in vitro Ellman's spectrophotometric and in situ bioautographic methods with physostigmine as standard. At least three morphological parts were examined for each of the plants investigated and the test concentration was 42.5 µg/ mL. Some plants were active on both enzymes though with some morphological parts being more active than others. The root bark of Spondias mombin showed the highest activity to the two enzymes; 64.77 percent and 83.94 percent on AChE and BuChE respectively. Other plant parts of the selected plants exhibited some remarkable selectivity in their actions. Those selectively active against AChE were Alchornia laxiflora stem bark (41.12 percent) and root bark, Callophyllum inophyllurn root bark (56.52 percent). The leaves of C. jagus (74.25 percent), Morinda lucida leaves (40.15 percent), Peltophorum pterocarpum leaves and stem bark (49.5 percent and 68.85 percent, respectively), physiostigmine gave 90.31 percent inhibition. Generally higher activities were found against BuChE. Bombax bromoposenze leaves, root bark and stem bark were particularly active. The inhibition was over 80 percent. Other selective plant parts are the leaves Antiaris africana, Cissampelos owarensis aerial parts (78.96 percent), Combretum molle leaves and stem bark (90.42 percent and 88.13 percent, respectively), Dioscorea dumentorum root bark and tuber (over 87 percent), G. kola leaves, Markhamia tomentosa root bark, Pycnanthus angolensis stem bark and Tetrapleura tetraptera leaves. Most of these plants are taken as food or are food ingredients in Nigeria and may account for the low incidence of Alzheimer's disease in the country and may play certain roles in the mediation of the disease.

As plantas podem ser úteis para estimular a memória, bem como serem usadas para combater o envelhecimento. Vinte e duas plantas, de dezesseis famílias, foram investigadas in vitro oara verificar sua atividade inibidora das enzimas acetilcolinesterase (AChE) e butirilcolinesterase (BuChE) pelo método espectrofotométrico de Ellman in situ e métodos de bioautografia utilizando fisostigmina como padrão. Pelo menos três partes morfológicas de cada planta foram analisadas e a concentração de ensaio foi de 42,5 µg/mL. Algumas plantas foram ativas em ambas as enzimas, embora com algumas partes mais ativas que outras. A casca da raiz de Spondias mombin apresentou a maior atividade as duas enzimas, 64,77 por cento para AChE e 83,94 por cento para BuChE. Outras partes das plantas selecionadas apresentaram boa seletividade em suas ações. As plantas seletivamente ativos contra AChE foram as casca do caule e casca da raiz de Alchornia laxiflora (41,12 por cento), e casca da raiz de Callophyllum inophyllurn (56,52 por cento). As folhas de C. jagus (74,25 por cento), folhas de Morinda lucida (40,15 por cento), folhas e casca do caule de Peltophorum pterocarpum (49,5 por cento e 68,85 por cento, respectivamente), physiostigmine inibiu 90,31 por cento. Em geral, atividades melhoras foram apresentadas contra BuChE. Folhas, casca da raiz e casca do caule Bombax bromoposenze foram particularmente ativos. A inibição foi acima de 80 por cento. Outras partes de algumas espécies também foram seletivas, como as partes aéreas de Antiaris africana, Cissampelos owarensis (78,96 por cento), folhas e casca do caule de Combretum molle (90,42 por cento e 88,13 por cento, respectivamente), casca da raiz e de tubérculos de Dioscorea dumentorum (mais de 87 por cento), folhas de G cola, cascas de raiz de Markhamia tomentosa, casca do caule de Pycnanthus angolensis e folhas de Tetrapleura tetraptera. A maioria destas plantas são utilizadas como alimentos ou ingredientes alimentares na Nigéria e podem ser responsáveis pela baixa incidência da doença de Alzheimer no país e desempenhar determinadas funções na mediação da doença.

A review on Alzheimer's disease: Its cause, symptoms, and treatment at world wide.

Is a progressive and fatal brain disease. As many as 5.3 million Americans are living with Alzheimer’s disease. Alzheimer's destroys brain cells, causing memory loss and problems with thinking and behavior severe enough to affect work, lifelong hobbies or social life. Alzheimer’s gets worse over time, and it is fatal. Today it is the seventh-leading cause of death in the United States. Learn more: Warning Signs and Stages of Alzheimer’s Disease. Has no current cure. But treatments for symptoms, combined with the right services and support, can make life better for the millions of Americans living with Alzheimer’s. There is an accelerating worldwide effort under way to find better ways to treat the disease, delay its onset, or prevent it from developing. Learn more about recent progress in Alzheimer research funded by the Alzheimer’s Association in the Research section.