Similar to cytokines above, quantitation revealed that vaccinatio

Similar to cytokines above, quantitation revealed that vaccinations did not increase the levels of salivary mucin expression, with, if anything, a decrease in mucin expression relative to infected, non-vaccinated mice (Fig. 4). Vaccination strategies against H. pylori have thus far proven inadequate PD0332991 due to their typical inability to reliably produce complete protection. The development

of a truly effective vaccine against H. pylori is severely hindered by our lack of understanding of host mechanisms involved in protective immunity against this infection. In this study we followed on from a previous observation by Shirai et al. which indicated that vaccine-mediated protection against H. pylori requires salivary glands, but for which a mechanism was lacking [11]. As the majority of H. pylori reside in mucus lining the gastric mucosa where they are exposed to secreted mucins, we theorized that mucin secretion by salivary HDAC inhibitors cancer glands could explain this observation. However, we found no evidence to suggest that vaccination produces any increase in immune response in the salivary glands. Cytokine and mucin expression levels were actually lower

in vaccinated/challenged mice compared with infected or uninfected controls, which in fact demonstrates an inverse correlation with the effector stage of protection. Shirai et al. concluded that salivary glands were important in the induction of protective

immunity, as sialoadenectomy 上海皓元 prior to vaccination against H. pylori removed vaccine efficacy [11]. However, they also found that salivary glands were important for long-term maintenance of vaccine-induced protection. The current study was not designed to evaluate the role of mucins in the initial induction of protective immunity, as we envisage that secreted salivary mucins are unlikely to play a role in immune induction. Hence a theoretical role for mucins in vaccine-mediated induction of protection against H. pylori cannot be completely ruled out by this study, although the mechanism by which this may occur is unclear. Rather, by their nature, we hypothesized that secreted salivary mucins may play an important role in the effector/maintenance stage of this protection; the data presented in this study argue against this theory. Another major product of salivary glands is immunoglobulin A (IgA) which is the main antibody isotype secreted into the gastrointestinal tract. The increased protein levels found in the salivary glands of vaccinated mice in this study correlated with an increase in IgA production which is completely consistent with current dogma regarding mucosal immune response to gastrointestinal vaccination and infection. This is further supported by Shirai et al., who showed that sialoadenectomized mice had less than half the levels of gastric and fecal IgA than did control animals [11].

Posted in Antibody | Leave a comment

Similar to cytokines above, quantitation revealed that vaccinatio

Similar to cytokines above, quantitation revealed that vaccinations did not increase the levels of salivary mucin expression, with, if anything, a decrease in mucin expression relative to infected, non-vaccinated mice (Fig. 4). Vaccination strategies against H. pylori have thus far proven inadequate this website due to their typical inability to reliably produce complete protection. The development

of a truly effective vaccine against H. pylori is severely hindered by our lack of understanding of host mechanisms involved in protective immunity against this infection. In this study we followed on from a previous observation by Shirai et al. which indicated that vaccine-mediated protection against H. pylori requires salivary glands, but for which a mechanism was lacking [11]. As the majority of H. pylori reside in mucus lining the gastric mucosa where they are exposed to secreted mucins, we theorized that mucin secretion by salivary Sirolimus datasheet glands could explain this observation. However, we found no evidence to suggest that vaccination produces any increase in immune response in the salivary glands. Cytokine and mucin expression levels were actually lower

in vaccinated/challenged mice compared with infected or uninfected controls, which in fact demonstrates an inverse correlation with the effector stage of protection. Shirai et al. concluded that salivary glands were important in the induction of protective

immunity, as sialoadenectomy 上海皓元 prior to vaccination against H. pylori removed vaccine efficacy [11]. However, they also found that salivary glands were important for long-term maintenance of vaccine-induced protection. The current study was not designed to evaluate the role of mucins in the initial induction of protective immunity, as we envisage that secreted salivary mucins are unlikely to play a role in immune induction. Hence a theoretical role for mucins in vaccine-mediated induction of protection against H. pylori cannot be completely ruled out by this study, although the mechanism by which this may occur is unclear. Rather, by their nature, we hypothesized that secreted salivary mucins may play an important role in the effector/maintenance stage of this protection; the data presented in this study argue against this theory. Another major product of salivary glands is immunoglobulin A (IgA) which is the main antibody isotype secreted into the gastrointestinal tract. The increased protein levels found in the salivary glands of vaccinated mice in this study correlated with an increase in IgA production which is completely consistent with current dogma regarding mucosal immune response to gastrointestinal vaccination and infection. This is further supported by Shirai et al., who showed that sialoadenectomized mice had less than half the levels of gastric and fecal IgA than did control animals [11].

Posted in Antibody | Leave a comment

Enzymes related to the

oxidative stress response, such as

Enzymes related to the

oxidative stress response, such as carbonyl reductase 3 (CBR3), or glutathione-S-transferase were more highly expressed in C3H/He mice on normal diet but were markedly increased in DDC-fed C57BL/6 mice. These data indicated profound alterations in basic biological processes in these mouse strains under basal conditions that could lay the foundation for different responses under disease conditions. Interestingly, some of these alterations (e.g., NDPK) were not seen at the messenger RNA (mRNA) expression level but only became evident after using a proteomics approach. Furthermore, in addition to the striking alteration of glyceraldehyde 3-phosphate dehydrogenase (GAPDH) expression, aggregation and nuclear translocation of this enzyme were observed. NDPH and GAPDH are of particular interest in the context of MDB pathogenesis. NDPK catalyzes the transfer of the PLX4032 terminal phosphate of nucleoside triphosphates to nucleoside diphosphates, thereby being important for the synthesis of GTP, CTP, and UTP. NDPK (also called Nm23) has been identified as a metastasis suppressor whose function is regulated by oxidation and reduction at its Cys109.7 GAPDH is best known as a glycolytic “housekeeping” cytoplasmic enzyme.

However, it appears to be involved in several additional GSK126 concentration processes such as DNA repair, transfer RNA (tRNA) export, membrane fusion, cytoskeletal dynamics, and cell death.8, 9 These different functions are, at least in part, regulated by oxidative stress, resulting in posttranslational modifications, oligomerization, aggregation, and nuclear translocation of GAPDH. To further understand the biological relevance of the strain-specific alterations of NDPK and GAPDH, a series of in vitro and ex vivo 上海皓元医药股份有限公司 experiments were performed by Snider et al. Using the reactive oxygen species (ROS)-sensitive fluorescent probe CM-H2DCFDA they demonstrated that DDC resulted in higher ROS levels in cultured C57BL/6 than in C3H/He hepatocytes. This increase in ROS was paralleled by an increase in CBR3 immunoreactivity, resembling the in vivo situation observed in livers of mice.

Furthermore, DDC treatment of hepatocytes isolated from C57BL/6 mice resulted in a dose-dependent reduction of cytoplasmic GAPDH and nuclear translocation which could be inhibited by pioglitazone. Using small interfering RNA (siRNA)-mediated knockdown, GAPDH was identified as an upstream regulator of NDPK and other enzymes involved in antioxidant responses. Consequently, knockdown of GAPDH or NDPK resulted in increased ROS formation in hepatocytes. Interestingly, knockdown of NDPK resulted also in a decrease of GAPDH, suggesting a coregulation of these two enzymes. The effects of GAPDH knockdown were not restricted to antioxidant enzymes but also affected metabolic functions, e.g., by down-regulation of fumarylacetoacetate hydrolase. The work of Snider et al.

Posted in Antibody | Leave a comment

Yakovlev Background: Ribavirin (RBV) can cause hemolytic anemia,

Yakovlev Background: Ribavirin (RBV) can cause hemolytic anemia, commonly managed by dose reduction. HCV-infected patients (pts) treated with the interferon-free 3 directacting antiviral (3D) regimen

of ABT-450 (identified by AbbVie and Enanta, dosed with ritonavir [r]), ombitasvir, and dasabuvir with RBV has demonstrated SVR12 rates of 92-96% among pts with cirrhosis treated for 12 or 24 weeks, respectively in the phase 3 TURQUIOSE-II trial. We describe the change in hemoglobin (Hgb) values and characteristics of cirrhotic pts requiring RBV dose reduction during treatment with 3D+RBV regimen. Methods: Patients with an adverse event (AE) this website requiring RBV dose modification were compared to those who did not. Stepwise logistic regression modeled RBV dose modification as the outcome variable. Risk variables in the regression model included prior pegIFN/RBV treatment experience, age,

sex, BMI, race, ethnicity, and baseline Hgb value, creatinine clearance (CrCl), platelet count, and albumin. Results: Of 380 pts treated with 3D+RBV, 39 (10.3%) required RBV dose modification due to an AE (37 [9.7%] related to Hgb reductions), PS-341 purchase including one serious AE of anemia; all achieved SVR12. Patients with RBV dose changes had lower mean baseline Hgb (13.7 vs. 15.0 g/ dL), lower

mean baseline CrCl (95.3 vs. 113.0 mL/min), and were older (60.7 vs. 56.4 years) than those not requiring dose changes. Women were more likely to require RBV dose reduction than men (19.5% vs. 6.4%, respectively). Lower baseline Hgb value and older age were significantly associated with increased risk for RBV dose modifications by regression analyses. Hemoglobin declines occurred primarily during the first 4 weeks of treatment with a mean decline of 3.1 g/dL in pts requiring RBV dose reduction and 1.9 g/dL in pts 上海皓元 without RBV dose reduction. 3 (1.4%) pts in the 12-week arm and 1 (0.6%) pt in the 24-week arm had Hgb declines below 8 g/dL. Hemoglobin returned to baseline values by post-treatment week 4. Conclusions: In cirrhotic pts, 3D+RBV led to low rates of anemia that resolved following treatment completion. Low baseline Hgb and older age predicted risk of AEs leading to RBV dose modification, which did not affect treatment response. Disclosures: Ira M.

Posted in Antibody | Leave a comment

Key Word(s): 1 Adipogenic; 2 Hepatocytes; 3 Cytokines; 4 NAFL

Key Word(s): 1. Adipogenic; 2. Hepatocytes; 3. Cytokines; 4. NAFLD; Presenting

Author: MARA BARBOSA Additional Authors: SILVIA LEITE, CARLA MARINHO, JOSE COTTER Corresponding Author: MARA BARBOSA Affiliations: CENTRO HOSPITALAR DO ALTO AVE – GASTROENTEROLOGY DEPARTMENT Objective: Recent data suggest that a decrease in liver elasticity is observed with increasing fibrosis in non-alcoholic fatty learn more liver disease (NAFLD). Metabolic syndrome is a known risk factor for non-alcoholic steatohepatitis and advanced fibrosis. To verify if metabolic syndrome is associated with a decrease in liver elasticity in NAFLD patients. To investigate the relationship between liver elasticity and demographic variables, body mass index (BMI), waist circumference and steatosis grade. Methods: Prospective study that included non-cirrhotic NAFLD patients. Variables analyzed: sex, age, metabolic syndrome (defined by NCEP/ATPIII criteria), ultrasound steatosis grade (classified as mild, moderate and severe) and liver elasticity (assessed by real-time find more elastography and defined by tissue mean elasticity (TME)). Statistical significance

was established at p < 0.05. Results: Thirty patients were evaluated, with 5 being excluded because of low-quality elastography information: 13 women, mean age of 53 years, mean BMI of 30 kg/m2, mean waist circumference of 101 cm. The prevalence of metabolic syndrome was 60% (n = 15). Steatosis

grade: mild in 13 patients, moderate in 10 and severe in 2. Mean TME was 105 ± 8. Patients with metabolic syndrome did not have lower TME values (105 vs 104; p = 0.848). TME showed a negative correlation with age (p = 0.026) and waist circumference (p = 0.013). TME values were higher in male patients (p = 0.007). TME did not correlate with BMI nor with steatosis grade (p = 0.131; p = 0.185). Conclusion: In NAFLD, liver elasticity assessed by real-time elastography inversely correlated with waist circumference and age. Nevertheless, there medchemexpress was no association with the presence of metabolic syndrome. Women had lower values of liver elasticity. Key Word(s): 1. elastography; 2. liver; 3. elasticity; 4. metabolic syndrome; Presenting Author: YING HU Additional Authors: HENGHUI ZHANG, JING LI, XU CONG, YANHUI CHEN, GAIXIA HE, YUJING CHI, YULAN LIU Corresponding Author: YULAN LIU Affiliations: Peking University People’s Hospital,; Peking University People’s Hospital, Peking University Hepatology Institute, Beijing Key Laboratory of Hepatitis C and Immunotherapy for Liver Diseases, Beijing 100044, P. R. China.; Department of Gastroenterology, Peking University People’s Hospital, Beijing100044, P. R. China.; Institute of Clinical Molecular Biology, Peking University People’s Hospital, Beijing 100044, P. R. China.; Department of Gastroenterology, Peking University People’s Hospital, Beijing 100044, P. R. China.

Posted in Antibody | Leave a comment

51 In patients with TERT or TERC mutations, aplastic

51 In patients with TERT or TERC mutations, aplastic Selleck R788 anemia or pulmonary fibrosis may be the only clinical presentation.11, 12 Most patients with telomerase mutations and aplastic anemia do not have respiratory failure, and most patients with pulmonary fibrosis do not have cytopenias, suggesting that environmental factors contribute to disease development in a susceptible patient; for example, most patients with telomerase mutations and pulmonary fibrosis are smokers.12, 13 In pedigrees of telomerase mutations, liver disease and aplastic anemia presented alone in different affected individuals, further suggesting a role for environmental factors. In one study, ≈3%

of patients with idiopathic pulmonary fibrosis also had cryptogenic cirrhosis, indicating some overlap between clinical features.52 Selleckchem AZD0530 In conclusion, telomerase mutations resulting in telomere erosion appear to be a genetic risk factor for human cirrhosis and may predispose affected subjects to disease progression in combination with environmental injury, further supporting telomere attrition as a causal event in cirrhosis pathophysiology. Establishing how shortened telomeres increase the risk of cirrhosis may allow for the design of future therapies to reduce the risk of hepatic fibrosis in susceptible populations. Patients with mutations

also may be appropriate targets for more aggressive forms of therapy to treat their primary disease given their increased risk of cirrhosis. Additional Supporting 上海皓元 Information may be found in the online version of this article. “
“Aim:  Several investigators have shown that interferon (IFN) therapy can suppress the recurrence of hepatocellular carcinoma (HCC) after curative treatment. We investigated the effect of IFN therapy on the first and second HCC recurrence following hepatic resection of

hepatitis C virus (HCV)-related HCC. Methods:  Subjects included 166 patients who had undergone curative resection for a single HCV-related HCC. We analyzed the outcome after initial hepatic resection and risk factors of a second HCC recurrence following treatment for the first HCC recurrence. Results:  Using multivariate analysis, a non-sustained virological response (non-SVR) was significantly associated with a high incidence of first HCC recurrence. The rate of second HCC recurrence tended to be higher in the non-SVR group than in the SVR group. In the patients with recurrence of multiple tumors or who received non-curative treatment for recurrent HCC, the second HCC recurrence rates were significantly higher. Multivariate analysis demonstrated that non-curative treatment for first HCC recurrence was an independent risk factor for a second HCC recurrence. Among the patients who received curative treatment for their first HCC recurrence, the rates of second recurrence were significantly higher in the non-SVR group than in the SVR group.

Posted in Antibody | Leave a comment

51 In patients with TERT or TERC mutations, aplastic

51 In patients with TERT or TERC mutations, aplastic 17-AAG datasheet anemia or pulmonary fibrosis may be the only clinical presentation.11, 12 Most patients with telomerase mutations and aplastic anemia do not have respiratory failure, and most patients with pulmonary fibrosis do not have cytopenias, suggesting that environmental factors contribute to disease development in a susceptible patient; for example, most patients with telomerase mutations and pulmonary fibrosis are smokers.12, 13 In pedigrees of telomerase mutations, liver disease and aplastic anemia presented alone in different affected individuals, further suggesting a role for environmental factors. In one study, ≈3%

of patients with idiopathic pulmonary fibrosis also had cryptogenic cirrhosis, indicating some overlap between clinical features.52 Selleck SCH 900776 In conclusion, telomerase mutations resulting in telomere erosion appear to be a genetic risk factor for human cirrhosis and may predispose affected subjects to disease progression in combination with environmental injury, further supporting telomere attrition as a causal event in cirrhosis pathophysiology. Establishing how shortened telomeres increase the risk of cirrhosis may allow for the design of future therapies to reduce the risk of hepatic fibrosis in susceptible populations. Patients with mutations

also may be appropriate targets for more aggressive forms of therapy to treat their primary disease given their increased risk of cirrhosis. Additional Supporting MCE公司 Information may be found in the online version of this article. “
“Aim:  Several investigators have shown that interferon (IFN) therapy can suppress the recurrence of hepatocellular carcinoma (HCC) after curative treatment. We investigated the effect of IFN therapy on the first and second HCC recurrence following hepatic resection of

hepatitis C virus (HCV)-related HCC. Methods:  Subjects included 166 patients who had undergone curative resection for a single HCV-related HCC. We analyzed the outcome after initial hepatic resection and risk factors of a second HCC recurrence following treatment for the first HCC recurrence. Results:  Using multivariate analysis, a non-sustained virological response (non-SVR) was significantly associated with a high incidence of first HCC recurrence. The rate of second HCC recurrence tended to be higher in the non-SVR group than in the SVR group. In the patients with recurrence of multiple tumors or who received non-curative treatment for recurrent HCC, the second HCC recurrence rates were significantly higher. Multivariate analysis demonstrated that non-curative treatment for first HCC recurrence was an independent risk factor for a second HCC recurrence. Among the patients who received curative treatment for their first HCC recurrence, the rates of second recurrence were significantly higher in the non-SVR group than in the SVR group.

Posted in Antibody | Leave a comment

51 In patients with TERT or TERC mutations, aplastic

51 In patients with TERT or TERC mutations, aplastic Quizartinib cell line anemia or pulmonary fibrosis may be the only clinical presentation.11, 12 Most patients with telomerase mutations and aplastic anemia do not have respiratory failure, and most patients with pulmonary fibrosis do not have cytopenias, suggesting that environmental factors contribute to disease development in a susceptible patient; for example, most patients with telomerase mutations and pulmonary fibrosis are smokers.12, 13 In pedigrees of telomerase mutations, liver disease and aplastic anemia presented alone in different affected individuals, further suggesting a role for environmental factors. In one study, ≈3%

of patients with idiopathic pulmonary fibrosis also had cryptogenic cirrhosis, indicating some overlap between clinical features.52 selleck chemicals In conclusion, telomerase mutations resulting in telomere erosion appear to be a genetic risk factor for human cirrhosis and may predispose affected subjects to disease progression in combination with environmental injury, further supporting telomere attrition as a causal event in cirrhosis pathophysiology. Establishing how shortened telomeres increase the risk of cirrhosis may allow for the design of future therapies to reduce the risk of hepatic fibrosis in susceptible populations. Patients with mutations

also may be appropriate targets for more aggressive forms of therapy to treat their primary disease given their increased risk of cirrhosis. Additional Supporting MCE Information may be found in the online version of this article. “
“Aim:  Several investigators have shown that interferon (IFN) therapy can suppress the recurrence of hepatocellular carcinoma (HCC) after curative treatment. We investigated the effect of IFN therapy on the first and second HCC recurrence following hepatic resection of

hepatitis C virus (HCV)-related HCC. Methods:  Subjects included 166 patients who had undergone curative resection for a single HCV-related HCC. We analyzed the outcome after initial hepatic resection and risk factors of a second HCC recurrence following treatment for the first HCC recurrence. Results:  Using multivariate analysis, a non-sustained virological response (non-SVR) was significantly associated with a high incidence of first HCC recurrence. The rate of second HCC recurrence tended to be higher in the non-SVR group than in the SVR group. In the patients with recurrence of multiple tumors or who received non-curative treatment for recurrent HCC, the second HCC recurrence rates were significantly higher. Multivariate analysis demonstrated that non-curative treatment for first HCC recurrence was an independent risk factor for a second HCC recurrence. Among the patients who received curative treatment for their first HCC recurrence, the rates of second recurrence were significantly higher in the non-SVR group than in the SVR group.

Posted in Antibody | Leave a comment

[32] The vast majority of migraine sufferers with CADASIL, 80-90%

[32] The vast majority of migraine sufferers with CADASIL, 80-90%, have migraine with aura.[27, 32] Rates of migraine without aura appear to be similar to the general population.[22] When migraine with aura is present, it is often the presenting symptom, and almost all migraine cases become symptomatic by age 38.[27] Aura characteristics are typical in 44% of cases, while 56% of cases also experience atypical features,

including aura without headache, brainstem aura, hemiplegic aura, prolonged Dasatinib order aura, or acute onset aura.[33] Severe attacks associated with fever, confusion, meningitis, or coma have also been reported.[34, 35] The frequency of attacks can be highly variable, and triggering factors are often typical for migraine headaches.[29] Subcortical ischemic events, whether transient ischemic events or completed infarctions, are the most frequent clinical manifestation of CADASIL, occurring in 65-85% of BGB324 manufacturer patients.27-29 The average incidence of

stroke in CADASIL patients is 10.4 per 100 person-years.[36] The age of onset of ischemic events is usually in the fifth decade of life, and most patients have recurrent ischemic events. Two-thirds of strokes correspond to classic lacunar syndromes, with the remainder representing mostly small deep infarctions.[22] Large artery infarcts are usually absent, although large vessels may occasionally be involved in CADASIL.[37] Traditional vascular risk factors are usually not present, although hypertension, high cholesterol, and smoking have been reported in case series.27-29 Cognitive dysfunction is the second most frequent clinical manifestation of CADASIL, being reported in 40-60% of patients in some case series.[27, 28, 38] Cognitive dysfunction typically is slowly progressive, and patients demonstrate a stepwise deterioration, typical for vascular dementia.[27, 29] It is by nature subcortical, and many patients have frontal lobe features, 上海皓元医药股份有限公司 such

as disinhibition, perseveration, and apathy. Most develop gait disturbance, urinary urgency, and pseudobulbar palsy as the disease progresses.27-29 One of the earliest signs of cognitive dysfunction is impairment in executive function and processing speed, almost universally present by age 50 in 1 case series of 42 symptomatic patients. Frank dementia appears later in the course of the disease, with 75% of demented patients being older than 60 years.[39] Mood disturbances are present in 20-30% of patients with CADASIL and most frequently present as episodes of severe depression, although manic episodes have also been described. Mood disturbances are rarely the presenting feature of the disorder, often developing as the disease progresses.27-29 Apathy, perhaps as a manifestation of frontal lobe symptoms seen with the development of dementia in these patients, has been described in 41% of patients and can occur independently from depression.

Posted in Antibody | Leave a comment

[32] The vast majority of migraine sufferers with CADASIL, 80-90%

[32] The vast majority of migraine sufferers with CADASIL, 80-90%, have migraine with aura.[27, 32] Rates of migraine without aura appear to be similar to the general population.[22] When migraine with aura is present, it is often the presenting symptom, and almost all migraine cases become symptomatic by age 38.[27] Aura characteristics are typical in 44% of cases, while 56% of cases also experience atypical features,

including aura without headache, brainstem aura, hemiplegic aura, prolonged AZD0530 manufacturer aura, or acute onset aura.[33] Severe attacks associated with fever, confusion, meningitis, or coma have also been reported.[34, 35] The frequency of attacks can be highly variable, and triggering factors are often typical for migraine headaches.[29] Subcortical ischemic events, whether transient ischemic events or completed infarctions, are the most frequent clinical manifestation of CADASIL, occurring in 65-85% of MK0683 solubility dmso patients.27-29 The average incidence of

stroke in CADASIL patients is 10.4 per 100 person-years.[36] The age of onset of ischemic events is usually in the fifth decade of life, and most patients have recurrent ischemic events. Two-thirds of strokes correspond to classic lacunar syndromes, with the remainder representing mostly small deep infarctions.[22] Large artery infarcts are usually absent, although large vessels may occasionally be involved in CADASIL.[37] Traditional vascular risk factors are usually not present, although hypertension, high cholesterol, and smoking have been reported in case series.27-29 Cognitive dysfunction is the second most frequent clinical manifestation of CADASIL, being reported in 40-60% of patients in some case series.[27, 28, 38] Cognitive dysfunction typically is slowly progressive, and patients demonstrate a stepwise deterioration, typical for vascular dementia.[27, 29] It is by nature subcortical, and many patients have frontal lobe features, 上海皓元 such

as disinhibition, perseveration, and apathy. Most develop gait disturbance, urinary urgency, and pseudobulbar palsy as the disease progresses.27-29 One of the earliest signs of cognitive dysfunction is impairment in executive function and processing speed, almost universally present by age 50 in 1 case series of 42 symptomatic patients. Frank dementia appears later in the course of the disease, with 75% of demented patients being older than 60 years.[39] Mood disturbances are present in 20-30% of patients with CADASIL and most frequently present as episodes of severe depression, although manic episodes have also been described. Mood disturbances are rarely the presenting feature of the disorder, often developing as the disease progresses.27-29 Apathy, perhaps as a manifestation of frontal lobe symptoms seen with the development of dementia in these patients, has been described in 41% of patients and can occur independently from depression.

Posted in Antibody | Leave a comment