An intracerebroventricular injection of AΒ (1-42) modifies temporal profiles of spatial memory performance and oxidative status in the temporal cortex rat.

Alzheimer's dementia (AD) is a neurodegenerative disorder that causes memory loss and dementia in older adults. Intracellular accumulation of Aß causes an imbalance in the oxidative status and cognitive dysfunctions. Besides oxidative stress and loss of memory, Alzheimer's patients show dysfunction of the circadian rhythms. The objective of this work was to evaluate the consequences of an intracerebroventricular injection of Aß (1-42) on temporal patterns of cognitive performance, as well as on lipid peroxidation, protein oxidation and total antioxidant capacity levels, in the rat temporal cortex. Holtzman male rats from control and Aß-injected groups were used in this study. We found that MDA, protein carbonyls and total antioxidant capacity levels displayed day-night oscillations in the rat temporal cortex and spatial memory performance also varied rhythmically. An intracerebroventricular injection of Aß (1-42) modified temporal patterns of cognitive performance as well as daily profiles of parameters of oxidative stress. Thus, elevated levels of Aß aggregates induces alterations in daily rhythmicity of parameters of oxidative stress and, consequently, would affect cellular clock activity, affecting the spatial memory performance in the AD.

Decreased hippocampal serotonin 5HT1A expression in mesial temporal lobe of epilepsy patients.

INTRODUCTION: Mesial temporal lobe epilepsy related to hippocampal sclerosis (MTLE-HS) is a surgically remediable epilepsy with a relatively high prevalence and psychiatric comorbidities. Depressive disorders may occur in up to 25% of MTLE-HS patients suggesting a common molecular mechanism underlying both conditions. OBJECTIVE: To compare the gene expression comprising serotonin 5HT1A and 5HT2A, noradrenaline (NA) ADRA1A, and ADRA2A receptors in the hippocampus of MTLE-HS patients with and without major depression. METHODS: A cross-sectional study allocated 31 patients in three groups: MTLE-HS without psychiatric diagnosis (MTLE-HS group), MTLE-HS with major depression (MTLE-HS-D group) and a control group consisting of healthy volunteers without any neurological or psychiatric disorders. Demographic and clinical characteristics were compared among groups. Gene expression of receptors were analyzed using general linear mixed models (GLMM), with an unstructured matrix, normal link. RESULTS: The three groups showed a similar distribution regarding age, gender (p > 0.16), history of initial precipitating injury, family history of epilepsy, monthly frequency of seizures, side of hippocampal sclerosis, interictal spike distribution and anti-seizure medications did not differ between MTLE-HS and MTLE-HS-D groups (p > 0.05). We observed a greater expression of the 5HT1A receptor in the control group when compared to the MTLE-HS (P = .004) and MTLE-HS-D (P = .007). Nevertheless, we did not observe any difference when MTLE-HS and MTLE-HS-D groups were compared to the controls for the ADRA1A (P = .931; P = .931), ADRA2A (P = .120; P = .121) and 5HT2A (P = .638; P = .318, respectively) gene expression. CONCLUSION: Mesial temporal lobe epilepsy related to hippocampal sclerosis and MTLE-HS-D patients showed a lowered expression of the 5HT1A receptors when compared with the controls adjusted for age and schooling. Data suggest that temporal lobe epilepsy plasticity may affect serotonin receptors, which may lead to more frequent cases of major depression in this population. More studies comprising wider samples are necessary to confirm these results; they also should investigate serotonin reuptake drugs as an adjuvant therapeutic option for MTLE-HS disorder.

Daily oscillation of cognitive factors is modified in the temporal cortex of an amyloid ß(1-42)-induced rat model of Alzheimer's disease.

Alzheimer's disease (AD) is a devastating disease characterized by loss of synapses and neurons in the elderly. Accumulation of the ß-amyloid peptide (Aß) in the brain is thought to be central to the pathogenesis of AD. ApoE plays a key role in normal and physiological clearance of Aß, since it facilitates the peptide intra- and extracellular proteolytic degradation. Besides the cognitive deficit, AD patients also show alterations in their circadian rhythms. The objective of this study was to investigate the effects of an i.c.v. injection of Aß (1-42) peptide on the 24 h rhythms of Apo E, BMAL1, RORα, Bdnf and trkB mRNA and Aß levels in the rat temporal cortex. We found that an i.c.v. injection of Aß aggregates phase shifts daily Bdnf expression as well as Apo E, BMAL1, RORα, Aß and decreased the mesor of TrkB rhythms. Thus, elevated Aß peptide levels might modify the temporal patterns of cognition-related factors, probably; by affecting the clock factors rhythms as well as in the 24 h rhythms of Apo E.

Depression and Temporal Lobe Epilepsy: Expression Pattern of Calbindin Immunoreactivity in Hippocampal Dentate Gyrus of Patients Who Underwent Epilepsy Surgery with and without Comorbid Depression.

PURPOSE: Changes in calbindin (CB) expression have been reported in patients with temporal lobe epilepsy (TLE) with controversial implications on hippocampal functions. The aim of this study was to determine the CB immunoreactivity in hippocampal dentate gyrus of patients who underwent epilepsy surgery for drug-resistant TLE with and without comorbid depression and/or memory deficits. METHODS: Selected hippocampal samples from patients with TLE who underwent epilepsy surgery were included. Clinical and complementary assessment: EEG, video-EEG, MRI, psychiatric assessment (structured clinical interview, DSM-IV), and memory assessment (Rey auditory verbal learning test, RAVLT; Rey-Osterrieth complex figure test, RCFT), were determined before surgery. Hippocampal sections were processed using immunoperoxidase with the anti-calbindin antibody. The semiquantitative analysis of CB immunoreactivity was determined in dentate gyrus by computerized image analysis (ImageJ). RESULTS: Hippocampal sections of patients with TLE and HS (n = 24) and postmortem controls (n = 5) were included. A significant reduction of CB+ cells was found in patients with TLE (p < 0.05, Student's t-test). Among TLE cases (n = 24), depression (n = 12) and memory deficit (n = 17) were determined. Depression was associated with a higher % of cells with the CB dendritic expression (CB-sprouted cells) (F(1, 20) = 11.81, p = 0.003, hp2 = 0.37), a higher CB+ area (µm2) (F(1, 20) = 5.33, p = 0.032, hp2 = 0.21), and a higher optical density (F(1, 20) = 15.09, p = 0.001, hp2 = 0.43) (two-way ANOVA). The GAF scale (general assessment of functioning) of DSM-IV inversely correlated with the % of CB-sprouted cells (r = -0.52, p = 0.008) and with the CB+ area (r = -0.46, p = 0.022). CONCLUSIONS: In this exploratory study, comorbid depression was associated with a differential pattern of CB cell loss in dentate gyrus combined with a higher CB sprouting. These changes may indicate granular cell dysmaturation associated to the epileptic hyperexcitability phenomena. Further investigations should be carried out to confirm these preliminary findings.

Mesenchymal stem cell therapy improves spatial memory and hippocampal structure in aging rats.

There is a growing interest in the potential of mesenchymal stem cells (MSCs) for implementing regenerative medicine in the brain as they have shown neurogenic and immunomodulatory activities. We assessed the effect of intracerebroventricular (icv) administration of human bone marrow-derived MSCs (hBM-MSCs) on spatial memory and hippocampal morphology of senile (27 months) female rats, using 3-months-old counterparts as young controls. Half of the animals were injected in the lateral ventricles (LV) with a suspension containing 5 × 105hBM-MSCs in 8 µl per side. The other half received no treatment (senile controls). Spatial memory performance was assessed with a modified version of the Barnes maze test. We employed one probe trial, one day after training in order to evaluate learning ability as well as spatial memory retention. Neuroblast (DCX) and microglial (Iba-1 immunoreactive) markers were also immunohistochemically quantitated in the animals by means of an unbiased stereological approach. In addition, hippocampal presynaptic protein expression was assessed by immunoblotting analysis. After treatment, the senile MSC-treated group showed a significant improvement in spatial memory accuracy and extended permanence in a one- and 3-hole goal sectors as compared with senile controls. The MSC treatment increased the number of neuroblasts in the hippocampal dentate gyrus, reduced the number of reactive microglial cells, and restored presynaptic protein levels as compared to senile controls. We conclude that icv injected hBM-MSCs are effective in improving spatial memory in senile rats and that the strategy improves some functional and morphologic brain features typically altered in aging rats.

Short-term high-fat diet modulates several inflammatory, ER stress, and apoptosis markers in the hippocampus of young mice.

The consumption of saturated fatty acids is one of the leading risk factors for Alzheimer's Disease (AD) development. Indeed, the short-term consumption of a high-fat diet (HFD) is related to increased inflammatory signals in the hippocampus; however, the potential molecular mechanisms linking it to AD pathogenesis are not fully elucidated. In our study, we investigated the effects of short-term HFD feeding (within 3, 7 and 10 days) in AD markers and neuroinflammation in the hippocampus of mice. The short period of HFD increased fasting glucose and HOMA-IR. Also, mice fed HFD increased the protein content of ß-Amyloid, pTau, TNFα, IL1ß, pJNK, PTP1B, peIF2α, CHOP, Caspase3, Cleaved-Caspase3 and Alzheimer-related genes (Bax, PS1, PEN2, Aph1b). At 10 days, both neuronal (N2a) and microglial (BV2) cells presented higher expression of inflammatory and apoptotic genes when stimulated with palmitate. These findings suggest that a short period of consumption of a diet rich in saturated fat is associated with activation of inflammatory, ER stress and apoptotic signals in the hippocampus of young mice.

The anticonvulsant effects of Ducrosia anethifolia (Boiss) essential oil are produced by its main component alpha-pinene in rats.

BACKGROUND: Ducrosia anethifolia has been recommended as a remedy for neurological disorders. However, the anticonvulsant effects of D. anethifolia essential oil (DAEO) and its major constituent α-pinene have not yet been clarified. METHODS: A rat model of pentylenetetrazole (PTZ)-induced convulsions was used. Oxidant and antioxidant parameters were assayed in the temporal lobe. RESULTS: The data showed that DAEO (50, 100 and 200 mg/kg, i.p.) and α-pinene (0.2 and 0.4 mg/kg i.p.) delayed the initiation time, and reduced the duration of myoclonic and tonic-clonic seizures following PTZ injection. The PTZ produced oxidative stress so that malondialdehyde and hydrogen peroxide levels were increased and catalase and peroxidase activity decreased. Pretreatment with DAEO and α-pinene significantly inhibited the above-mentioned enzymatic changes in PTZ-treated animals. CONCLUSION: The results suggest that α-pinene, at teast in part, was responsible for the induction of the anticonvulsant and antioxidant effects of DAEO in rats.

Anorexia increases microglial density and cytokine expression in the hippocampus of young female rats.

Anorexia by osmotic dehydration is an adaptive response to hypernatremia and hyperosmolaemia induced by ingestion of a hypertonic solution. Dehydration-induced anorexia (DIA) reproduces weight loss and avoidance of food, despite its availability. By using this model, we previously showed increased reactive astrocyte density in the rat dorsal hippocampus, suggesting a pro-inflammatory environment where microglia may play an important role. However, whether such anorexic condition increases a pro-inflammatory response is unknown. The aim of this study was to test if DIA increases microglial density in the dorsal hippocampus, as well as the expression of pro-inflammatory cytokines tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6) and interleukin 1 beta (IL-1ß) in the hippocampus of young female rats. Our results showed that DIA significantly increased microglial density in CA2-CA3 and dentate gyrus (DG) but not in CA1. However, forced food restriction (FFR) only increased microglial density in the DG. Accordingly, the activated/resting microglia ratio was significantly increased in CA2-CA3 and DG, in DIA and FFR groups. Finally, western blot analysis showed increased expression of IBA1, TNF-α, IL-6 and IL-1ß in the hippocampus of both experimental groups. We conclude that anorexia triggers increased reactive microglial density and expression of TNF-α, IL-6 and IL-1ß; this environment may result in hippocampal neuroinflammation.

Glycosaminoglycans from Alzheimer's disease hippocampus have altered capacities to bind and regulate growth factors activities and to bind tau.

Glycosaminoglycans (GAGs), including heparan sulfates and chondroitin sulfates, are major components of the extracellular matrix. Upon interacting with heparin binding growth factors (HBGF), GAGs participate to the maintaintenance of tissue homeostasis and contribute to self-healing. Although several processes regulated by HBGF are altered in Alzheimer's disease, it is unknown whether the brain GAG capacities to bind and regulate the function of HBGF or of other heparin binding proteins, as tau, are modified in this disease. Here, we show that total sulfated GAGs from hippocampus of Alzheimer's disease have altered capacities to bind and potentiate the activities of growth factors including FGF-2, VEGF, and BDNF while their capacity to bind to tau is remarkable increased. Alterations of GAG structures and capacities to interact with and regulate the activity of heparin binding proteins might contribute to impaired tissue homeostasis in the Alzheimer's disease brain.

Lower mitochondrial DNA content but not increased mutagenesis associates with decreased base excision repair activity in brains of AD subjects.

Accumulation of oxidative mitochondrial DNA (mtDNA) damage and impaired base excision repair (BER) in brains have been associated with Alzheimer's disease (AD). However, it is still not clear how these affect mtDNA stability, as reported levels of mtDNA mutations in AD are conflicting. Thus, we investigated whether alterations in BER correlate with mtDNA instability in AD using postmortem brain samples from cognitively normal AD subjects and individuals who show neuropathological features of AD, but remained cognitively normal (high-pathology control). To date, no data on DNA repair and mtDNA stability are available for these individuals. BER activities, mtDNA mutations, and mtDNA copy number were measured in the nuclear and mitochondrial extracts. Significantly lower uracil DNA glycosylase activity was detected in nuclear and mitochondrial extracts from AD subjects, while apurinic/apyrimidinic endonuclease activity was similar in all groups. Although mtDNA mutation frequency was similar in all groups, mtDNA copy number was significantly decreased in the temporal cortex of AD brains but not of high-pathology control subjects. Our results show that lower mitochondrial uracil DNA glycosylase activity does not result in increased mutagenesis, but rather in depletion of mtDNA in early-affected brain regions during AD development.

Intrinsic and synaptic properties of hippocampal CA1 pyramidal neurons of the Wistar Audiogenic Rat (WAR) strain, a genetic model of epilepsy.

Despite the many studies focusing on epilepsy, a lot of the basic mechanisms underlying seizure susceptibility are mainly unclear. Here, we studied cellular electrical excitability, as well as excitatory and inhibitory synaptic neurotransmission of CA1 pyramidal neurons from the dorsal hippocampus of a genetic model of epilepsy, the Wistar Audiogenic Rat (WARs) in which limbic seizures appear after repeated audiogenic stimulation. We examined intrinsic properties of neurons, as well as EPSCs evoked by Schaffer-collateral stimulation in slices from WARs and Wistar parental strain. We also analyzed spontaneous IPSCs and quantal miniature inhibitory events. Our data show that even in the absence of previous seizures, GABAergic neurotransmission is reduced in the dorsal hippocampus of WARs. We observed a decrease in the frequency of IPSCs and mIPSCs. Moreover, mIPSCs of WARs had faster rise times, indicating that they probably arise from more proximal synapses. Finally, intrinsic membrane properties, firing and excitatory neurotransmission mediated by both NMDA and non-NMDA receptors are similar to the parental strain. Since GABAergic inhibition towards CA1 pyramidal neurons is reduced in WARs, the inhibitory network could be ineffective to prevent the seizure-dependent spread of hyperexcitation. These functional changes could make these animals more susceptible to the limbic seizures observed during the audiogenic kindling.

Differential Pattern of Phospholipid Profile in the Temporal Cortex from E280A-Familiar and Sporadic Alzheimer's Disease Brains.

Lipids are considered important factors in the pathogenesis of Alzheimer's disease (AD). In this study, we realized a comparative analysis of the phospholipid profile and phospholipid composition of the temporal cortex from E280A-familiar AD (FAD), sporadic AD (SAD), and healthy human brains. Findings showed a significant decrease of lysophosphatidylcholine and phosphatidylethanolamine formed by low levels of polyunsaturated fatty acids (20 : 4, 22 : 6) in AD brains. However, phosphatidylethanolamine-ceramide and phosphoglycerol were significantly increased in SAD, conformed by high levels of (18 : 0/18 : 1) and (30/32/36 : 0/1/2), respectively. Together, the findings suggest a deficiency in lysophosphacholine and phosphatidylethanolamine, and alteration in the balance between poly- and unsaturated fatty acids in both types of AD, and a differential pattern of phospholipid profile and fatty acid composition between E280A FAD and SAD human brains.

Neuroinflammation induced by amyloid ß25-35 modifies mucin-type O-glycosylation in the rat's hippocampus.

Amyloid-ß (Aß) plays a relevant role in the neurodegenerative process of Alzheimer's disease (AD). The 25-35 peptide of amyloid-ß (Aß25-35) induces the inflammatory response in brain experimental models. Mucin-type O-glycosylation has been associated with inflammation of brain tissues in AD, thus in this work, we aimed at identifying changes in the glycosylation profile generated by the injection of Aß25-35 into the CA1 of the hippocampus of rats, using histochemistry with lectins. Our results indicate that 100µM Aß25-35 induce increased recognition of the Amaranthus leucocarpus lectin (ALL) (specific for Galß1,3-GalNAcα1,0-Ser/Thr); whereas concanavalin A (Con A) (specific for α-Man) showed no differences among treated and control groups of rats. Jacalin and peanut agglutinin (Galß1,3GalNAcα1,0-Ser/Thr) showed no recognition of brain cells of control or treated rats. After 6-h treatment of the tissue with trypsin or with 200mM GalNAc, the interaction with ALL was inhibited. Immunohistochemistry showed positive anti-NeuN and ALL-recognition of neurons; however, anti-GFAP and anti-CD11b showed no co-localization with ALL. The ALL+ neurons revealed the presence of cytochrome C in the cytosol and active caspase 3 in the cytosol and nucleus. Administration of the interleukin-1 receptor antagonist (IL-1RA) to Aß25-35-treated rats diminished neuroinflammation and ALL recognition. These results suggest a close relationship among over-expression of mucin-type O-glycosylation, the neuroinflammatory process, and neuronal death.

Immunohistochemical study of Metallothionein in patients with temporal lobe epilepsy.

Epilepsy is characterized by spontaneous recurrent seizures and temporal lobe epilepsy (TLE) is the most common serious neurological example of acquired and frequent epilepsy. Oxidative stress is recognized as playing a contributing role in several neurological disorders, and most recently have been implicated in acquired epilepsies. The MTs occur in several brain regions and may serve as neuroprotective proteins against reactive oxygen species causing oxidative damage and stress. The main aim of this work was to describe the immunohistochemical localization of MT in the specimens derived from the patients affected by TLE. Histopathological examination showed NeuN, GFAP and MT immunopositive cells that were analyzed for determinate in hippocampal and parietal cortex samples. An increase in the reactive gliosis associated with increased MT expression was observed in patients with TLE.

Differential DNA Methylation of MicroRNA Genes in Temporal Cortex from Alzheimer's Disease Individuals.

This study investigated for the first time the genomewide DNA methylation changes of noncoding RNA genes in the temporal cortex samples from individuals with Alzheimer's disease (AD). The methylome of 10 AD individuals and 10 age-matched controls were obtained using Illumina 450 K methylation array. A total of 2,095 among the 15,258 interrogated noncoding RNA CpG sites presented differential methylation, 161 of which were associated with miRNA genes. In particular, 10 miRNA CpG sites that were found to be hypermethylated in AD compared to control brains represent transcripts that have been previously associated with the disease. This miRNA set is predicted to target 33 coding genes from the neuregulin receptor complex (ErbB) signaling pathway, which is required for the neurons myelination process. For 6 of these miRNA genes (MIR9-1, MIR9-3, MIR181C, MIR124-1, MIR146B, and MIR451), the hypermethylation pattern is in agreement with previous results from literature that shows downregulation of miR-9, miR-181c, miR-124, miR-146b, and miR-451 in the AD brain. Our data implicate dysregulation of miRNA methylation as contributor to the pathogenesis of AD.

Extratemporal abnormalities in phosphorus magnetic resonance spectroscopy of patients with mesial temporal sclerosis.

OBJECTIVE: We evaluated extratemporal metabolic changes with phosphorus magnetic resonance spectroscopy (31P-MRS) in patients with unilateral mesial temporal sclerosis (MTS). METHOD: 31P-MRS of 33 patients with unilateral MTS was compared with 31 controls. The voxels were selected in the anterior, posterior insula-basal ganglia (AIBG, PIBG) and frontal lobes (FL). Relative values of phosphodiesters- PDE, phosphomonoesters-PME, inorganic phosphate - Pi, phosphocreatine- PCr, total adenosine triphosphate [ATPt = γ- + a- + b-ATP] and the ratios PCr/ATPt, PCr/γ-ATP, PCr/Pi and PME/PDE were obtained. RESULTS: We found energetic abnormalities in the MTS patients compared to the controls with Pi reduction bilaterally in the AIBG and ipsilaterally in the PIBG and the contralateral FL; there was also decreased PCr/γ-ATP in the ipsilateral AIBG and PIBG. Increased ATPT in the contralateral AIBG and increased γ-ATP in the ipsilateral PIBG were detected. CONCLUSION: Widespread energy dysfunction was detected in patients with unilateral MTS.

Pharmacoresistant temporal lobe epilepsy modifies histamine turnover and H3 receptor function in the human hippocampus and temporal neocortex.

Experiments were designed to evaluate the tissue content of tele-methylhistamine (t-MeHA) and histamine as well as H3 receptor (H3 Rs) binding and activation of the heterotrimeric guanine nucleotide binding αi/o proteins (Gαi/o) coupled to these receptors in the hippocampus and temporal neocortex of patients (n = 10) with pharmacoresistant mesial temporal lobe epilepsy (MTLE). Patients with MTLE showed elevated tissue content of t-MeHA in the hippocampus. Analyses revealed that a younger age at seizure onset was correlated with a higher tissue content of t-MeHA, lower H3 R binding, and lower efficacy of Gαi/o protein activation in the hippocampus. We conclude that the hippocampus shows a reduction in the H3 R function associated with enhanced histamine. In contrast, the temporal neocortex displayed a high efficacy of H3 Rs Gαi/o protein activation that was associated with low tissue contents of histamine and t-MeHA. These results indicate an overactivation of H3 Rs leading to decreased histamine in the temporal neocortex. However, this situation was lessened in circumstances such as a longer duration of epilepsy or higher seizure frequency. It is concluded that decrease in H3 Rs function and enhanced levels of histamine may contribute to the epileptic activity in the hippocampus and temporal neocortex of patients with pharmacoresistant MTLE.

Extratemporal abnormalities in phosphorus magnetic resonance spectroscopy of patients with mesial temporal sclerosis / Anormalidades extratemporais na espectroscopia de fósforo por ressonância magnética em pacientes com esclerose mesial temporal

ABSTRACT Objective We evaluated extratemporal metabolic changes with phosphorus magnetic resonance spectroscopy (31P-MRS) in patients with unilateral mesial temporal sclerosis (MTS). Method 31P-MRS of 33 patients with unilateral MTS was compared with 31 controls. The voxels were selected in the anterior, posterior insula-basal ganglia (AIBG, PIBG) and frontal lobes (FL). Relative values of phosphodiesters- PDE, phosphomonoesters-PME, inorganic phosphate - Pi, phosphocreatine- PCr, total adenosine triphosphate [ATPt = γ- + a- + b-ATP] and the ratios PCr/ATPt, PCr/γ-ATP, PCr/Pi and PME/PDE were obtained. Results We found energetic abnormalities in the MTS patients compared to the controls with Pi reduction bilaterally in the AIBG and ipsilaterally in the PIBG and the contralateral FL; there was also decreased PCr/γ-ATP in the ipsilateral AIBG and PIBG. Increased ATPT in the contralateral AIBG and increased γ-ATP in the ipsilateral PIBG were detected. Conclusion Widespread energy dysfunction was detected in patients with unilateral MTS.

RESUMO Objetivo Nós avaliamos as alterações metabóblicas através da espectroscopia de fósforo por ressonância magnética (31P-MRS) em pacientes com esclerose mesial temporal (EMT) unilateral. Método 31P-MRS de 33 pacientes com EMT unilateral foram comparadas aos de 31 controles. Foram selecionados os voxels nas regiões insulonuclear anterior e posterior (RINA e RINP) e frontal (RF). Os valores relativos de fosfodiésteres – PDE, fosfomonoésteres- PME, fosfato inorgânico- Pi, fosfocreatina –PCr, adenosina trifosfato total [ATPt = γ- + a- + b-ATP] e as razões PCr/ATPt, PCr/γ-ATP, PCr/Pi e PME/PDE foram obtidas. Resultados Nós encontramos anormalidades em pacientes com EMT em comparação aos controles. Redução de Pi nas RINA bilateralmente, RINP ipsilateral e RF contralateral, redução de PCr/γ-ATP nas RINA e RINP ipsilaterais foram detectadas. Aumentos de ATPT na RINA contralateral e aumento de γ-ATP na RINP ipsilateral também foram encontradas. Conclusão Disfunção energética difusa foi encontrada em pacientes com EMT unilateral.

A high calorie diet causes memory loss, metabolic syndrome and oxidative stress into hippocampus and temporal cortex of rats.

A high calorie intake can induce the appearance of the metabolic syndrome (MS), which is a serious public health problem because it affects glucose levels and triglycerides in the blood. Recently, it has been suggested that MS can cause complications in the brain, since chronic hyperglycemia and insulin resistance are risk factors for triggering neuronal death by inducing a state of oxidative stress and inflammatory response that affect cognitive processes. This process, however, is not clear. In this study, we evaluated the effect of the consumption of a high-calorie diet (HCD) on both neurodegeneration and spatial memory impairment in rats. Our results demonstrated that HCD (90 day consumption) induces an alteration of the main energy metabolism markers, indicating the development of MS in rats. Moreover, an impairment of spatial memory was observed. Subsequently, the brains of these animals showed activation of an inflammatory response (increase in reactive astrocytes and interleukin1-ß as well as tumor necrosis factor-α) and oxidative stress (reactive oxygen species and lipid peroxidation), causing a reduction in the number of neurons in the temporal cortex and hippocampus. Altogether, these results suggest that a HCD promotes the development of MS and contributes to the development of a neurodegenerative process and cognitive failure. In this regard, it is important to understand the relationship between MS and neuronal damage in order to prevent the onset of neurodegenerative disorders.

Visual hallucinations of autobiographic memory and asomatognosia: a case of epilepsy due to brain cysticercosis.

The current study describes the case of a woman with symptomatic epilepsy due to brain cysticercosis acquired during childhood. During her adolescence, she developed seizures characterized by metamorphopsia, hallucinations of autobiographic memory and, finally, asomatognosia. Magnetic brain imaging showed a calcified lesion in the right occipitotemporal cortex, and positron emission tomography imaging confirmed the presence of interictal hypometabolism in two regions: the right parietal cortex and the right lateral and posterior temporal cortex. We discuss the link between these brain areas and the symptoms described under the concepts of epileptogenic lesion, epileptogenic zone, functional deficit zone, and symptomatogenic zone.