Pub Date : 2017-02-28DOI: 10.4172/2161-0460.1000306
Alex, re Mello, Marina Rocha Frusciante, Luciana Gonçalves Kneib, Gabrielli Bortolato, Jaqueline Cé, C. Dani, C. Funchal, J. Coelho
Objective: Pompe disease is an autosomal recessive disorder of lysosomal storage, caused by the deficiency of α-glucosidase lysosomal enzymes. Several studies have demonstrated the involvement of oxidative stress in numerous pathophysiological changes. To assess parameters of oxidative stress in patients with Pompe’s disease (PD) and in normal controls, establishing a possible analysis of the differences between both groups. Methods: Evaluation, in plasma samples and leukocytes, of the enzyme activities of α-glucosidase, of antioxidants SOD1 and CAT enzymes, as well as the levels of lipid peroxidation (TBARS), protein damage (carbonyl) and non-enzymatic antioxidant (sulphydryl) defenses on samples of 10 individuals with PD (4 women and 6 men) and 10 healthy individuals. Results: There was a reduction in the enzymatic activity of α-glucosidase in samples of leukocytes of patients with PD compared to samples from normal subjects, confirming the deficiency of this enzyme. With respect to oxidative stress, there was an increase of carbonyl groups in the plasma of the PD patients studied relative to controls, suggesting oxidative damage to proteins. No differences were observed between the two groups for the remaining oxidative stress parameters evaluated. Discussion: We conclude, therefore, that the presence of PD is a significant factor to increase the oxidative stress levels, with no change in levels of antioxidant enzymes. It is suggested that further studies with other lysosomal storage diseases be carried out in order to propose, in the future, antioxidant therapies to prevent protein damage.
{"title":"ÃÂ-Glucosidase Deficiency Promotes Increasing Protein Oxidative Damagein Pompe Disease Patients","authors":"Alex, re Mello, Marina Rocha Frusciante, Luciana Gonçalves Kneib, Gabrielli Bortolato, Jaqueline Cé, C. Dani, C. Funchal, J. Coelho","doi":"10.4172/2161-0460.1000306","DOIUrl":"https://doi.org/10.4172/2161-0460.1000306","url":null,"abstract":"Objective: Pompe disease is an autosomal recessive disorder of lysosomal storage, caused by the deficiency of α-glucosidase lysosomal enzymes. Several studies have demonstrated the involvement of oxidative stress in numerous pathophysiological changes. To assess parameters of oxidative stress in patients with Pompe’s disease (PD) and in normal controls, establishing a possible analysis of the differences between both groups. Methods: Evaluation, in plasma samples and leukocytes, of the enzyme activities of α-glucosidase, of antioxidants SOD1 and CAT enzymes, as well as the levels of lipid peroxidation (TBARS), protein damage (carbonyl) and non-enzymatic antioxidant (sulphydryl) defenses on samples of 10 individuals with PD (4 women and 6 men) and 10 healthy individuals. Results: There was a reduction in the enzymatic activity of α-glucosidase in samples of leukocytes of patients with PD compared to samples from normal subjects, confirming the deficiency of this enzyme. With respect to oxidative stress, there was an increase of carbonyl groups in the plasma of the PD patients studied relative to controls, suggesting oxidative damage to proteins. No differences were observed between the two groups for the remaining oxidative stress parameters evaluated. Discussion: We conclude, therefore, that the presence of PD is a significant factor to increase the oxidative stress levels, with no change in levels of antioxidant enzymes. It is suggested that further studies with other lysosomal storage diseases be carried out in order to propose, in the future, antioxidant therapies to prevent protein damage.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"6 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2017-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72761991","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Parkinson disease (PD) is the second most common neurodegenerative disorder after Alzheimer disease with no definitive neuroprotective therapies. Previous studies have demonstrated that Catechol tetra hydroisoquinolines (CTIQs) are toxic to dopaminergic neurons. These toxins can induce mitochondrial dysfunction, which consequently contributes to the pathogenesis of PD. Unlike external neurotoxins, such as agrochemicals and MPTP, CTIQs can be synthesized in the brains of human based on the dopamine and the particular aldehyde. Besides, aggregated α-synuclein (α-syn), one of the hallmarks of PD, has been proved to be a key contributor in the development of PD and can be affected by many neurotoxins. Some studies have presented that CTIQs enhanced the aggregation of α-syn and increased the neurotoxin of α-syn, which might be the pathological mechanism of PD. Therefore, this chapter will reveal the role of CTIQs and α-syn and try to clarify the relationship between them.
{"title":"Catechol Tetrahydroisoquinolines Enhance a-Synuclein Aggregation andSpecify the Neurotoxicity to Dopaminergic Neurons","authors":"Zixuan Chen, Jian-jun Lu, Jinyan Duan, Xiaotong Zheng, Yanyan Zhang, Chao Han, Yulin Deng","doi":"10.4172/2161-0460.1000308","DOIUrl":"https://doi.org/10.4172/2161-0460.1000308","url":null,"abstract":"Parkinson disease (PD) is the second most common neurodegenerative disorder after Alzheimer disease with no definitive neuroprotective therapies. Previous studies have demonstrated that Catechol tetra hydroisoquinolines (CTIQs) are toxic to dopaminergic neurons. These toxins can induce mitochondrial dysfunction, which consequently contributes to the pathogenesis of PD. Unlike external neurotoxins, such as agrochemicals and MPTP, CTIQs can be synthesized in the brains of human based on the dopamine and the particular aldehyde. Besides, aggregated α-synuclein (α-syn), one of the hallmarks of PD, has been proved to be a key contributor in the development of PD and can be affected by many neurotoxins. Some studies have presented that CTIQs enhanced the aggregation of α-syn and increased the neurotoxin of α-syn, which might be the pathological mechanism of PD. Therefore, this chapter will reveal the role of CTIQs and α-syn and try to clarify the relationship between them.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"10 1","pages":"1-12"},"PeriodicalIF":0.0,"publicationDate":"2017-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78571721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-02-23DOI: 10.4172/2161-0460.1000305
H. Kaneto, T. Kinoshita, M. Shimoda, K. Kaku
The number of subjects with dementia has been increasing all over the world which has become one of the serious social issues. Mainly, there are two types of dementia; one type is Alzheimer’s disease and another type is vascular dementia. Such dementia is often complicated in elderly subjects with diabetes and thereby it is thought that dementia is one of diabetic complications. There are many possible explanation about the mechanism by which dementia is easily induced in subjects with diabetes. Chronic hyperglycemia and repeated hypoglycemia are closely associated with the onset and/or development of dementia. In addition, the fluctuation of blood glucose level per se is also associated with dementia. In this review article, we would like to describe the current status of dementia and association between dementia and diabetes.
{"title":"The Presence of Dementia as one of Diabetic Complications: Hyperglycemia, Hypoglycemia and Glycemic Fluctuation are Associated with the Development of Dementia","authors":"H. Kaneto, T. Kinoshita, M. Shimoda, K. Kaku","doi":"10.4172/2161-0460.1000305","DOIUrl":"https://doi.org/10.4172/2161-0460.1000305","url":null,"abstract":"The number of subjects with dementia has been increasing all over the world which has become one of the serious social issues. Mainly, there are two types of dementia; one type is Alzheimer’s disease and another type is vascular dementia. Such dementia is often complicated in elderly subjects with diabetes and thereby it is thought that dementia is one of diabetic complications. There are many possible explanation about the mechanism by which dementia is easily induced in subjects with diabetes. Chronic hyperglycemia and repeated hypoglycemia are closely associated with the onset and/or development of dementia. In addition, the fluctuation of blood glucose level per se is also associated with dementia. In this review article, we would like to describe the current status of dementia and association between dementia and diabetes.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"93 11 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2017-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91079734","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-02-22DOI: 10.4172/2161-0460.1000304
C. Gennaro, Levantesi Laura, Oggiano Marco, Sicuranza Rossella, Congedo Elisabetta, D. Germano
Postoperative cognitive dysfunction (POCD) results as a large problem that causes a reduction in the quality of life and increases morbidity and mortality especially in elderly patients. The increased age of patients undergoing surgery has made evident the problem and several studies evaluated pathogenesis and implemented a targeted therapy. This review analyses POCD, delirium and mild cognitive impairment (MCI) definition, risk factors and physiopathology with an analysis on anaesthesia technique influence. Unlike the postoperative delirium, POCD is more difficult to diagnose because of several tests that must be administered in the pre and postoperative period, even at a distance of time. Furthermore adequate depth of anaesthesia, monitored with Bispectral Index (BIS) or Electroencephalography (EEG), reduces the cognitive dysfunction incidence. Currently the pathogenesis is not well understood although neuro inflammation plays a central role while the importance of anaesthesia techniques has not established.
{"title":"Cognitive Dysfunction after Surgery: An Emergent Problem","authors":"C. Gennaro, Levantesi Laura, Oggiano Marco, Sicuranza Rossella, Congedo Elisabetta, D. Germano","doi":"10.4172/2161-0460.1000304","DOIUrl":"https://doi.org/10.4172/2161-0460.1000304","url":null,"abstract":"Postoperative cognitive dysfunction (POCD) results as a large problem that causes a reduction in the quality of life and increases morbidity and mortality especially in elderly patients. The increased age of patients undergoing surgery has made evident the problem and several studies evaluated pathogenesis and implemented a targeted therapy. This review analyses POCD, delirium and mild cognitive impairment (MCI) definition, risk factors and physiopathology with an analysis on anaesthesia technique influence. Unlike the postoperative delirium, POCD is more difficult to diagnose because of several tests that must be administered in the pre and postoperative period, even at a distance of time. Furthermore adequate depth of anaesthesia, monitored with Bispectral Index (BIS) or Electroencephalography (EEG), reduces the cognitive dysfunction incidence. Currently the pathogenesis is not well understood although neuro inflammation plays a central role while the importance of anaesthesia techniques has not established.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"2 1","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"2017-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78314100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-02-04DOI: 10.4172/2161-0460.1000302
Annika Philipps, S. Müller, O. Preische, C. Laske
Objective: Subjective Cognitive Decline (SCD) is actually considered to be associated with an increased likelihood of future cognitive impairment and dementia. Much less is known about worries concerning Alzheimer’s disease (AD Worry) and their relation to SCD, SCD with worries (SCD+Worry) and objective cognitive performance. Methods: We examined the prevalence and relation of AD Worry, SCD and SCD+Worry along with cognitive measures (MMSE, DemTect) among 100 proxies of persons with AD and 119 age-, gender- and education-matched controls. Results: AD Worry, SCD and SCD+Worry were frequently present in proxies of persons with AD (64.0%/47.0%/21.0%) and controls (62.2%/51.3%/16.8%) without significant group differences concerning frequency of occurrence and cognitive measures. Among proxies of AD patients, AD Worry occurred more frequently in first degree relatives (sons/daughters; 76.5%) compared to spouses (45.5%; p=0.002). Proxies with AD Worry were significantly younger (58.9 years) than proxies with SCD+Worry (67.4 years; p=0.012). Proxies of AD patients with feelings of burden reported SCD (55.6%) significantly more frequently than proxies without feelings of burden (32.4%; p=0.025). Controls with AD Worry reported SCD+Worry (23.0%) significantly more frequently compared to controls without AD Worry (6.7%; p=0.021). In line with the latter result, there was a significant positive correlation between AD Worry and SCD+Worry (r=0.211, p=0.021) in the control sample. Conclusion: AD Worry is a widespread phenomenon within the examined cohorts of proxies of AD patients and controls. It is not associated with objective cognitive impairment. However, the higher presence of SCD+Worry in those controls who reported AD Worry and the higher presence of AD Worry among sons and daughters of AD patients compared to spouses indicate that AD Worry could be an early indicator of future cognitive impairment. Longitudinal studies examining larger samples are needed to further elucidate the potential association between AD Worry, SCD and future cognitive decline.
{"title":"Worries about Alzheimer's Disease and Subjective Cognitive Decline in Proxies of AD Patients and Controls","authors":"Annika Philipps, S. Müller, O. Preische, C. Laske","doi":"10.4172/2161-0460.1000302","DOIUrl":"https://doi.org/10.4172/2161-0460.1000302","url":null,"abstract":"Objective: Subjective Cognitive Decline (SCD) is actually considered to be associated with an increased likelihood of future cognitive impairment and dementia. Much less is known about worries concerning Alzheimer’s disease (AD Worry) and their relation to SCD, SCD with worries (SCD+Worry) and objective cognitive performance. Methods: We examined the prevalence and relation of AD Worry, SCD and SCD+Worry along with cognitive measures (MMSE, DemTect) among 100 proxies of persons with AD and 119 age-, gender- and education-matched controls. Results: AD Worry, SCD and SCD+Worry were frequently present in proxies of persons with AD (64.0%/47.0%/21.0%) and controls (62.2%/51.3%/16.8%) without significant group differences concerning frequency of occurrence and cognitive measures. Among proxies of AD patients, AD Worry occurred more frequently in first degree relatives (sons/daughters; 76.5%) compared to spouses (45.5%; p=0.002). Proxies with AD Worry were significantly younger (58.9 years) than proxies with SCD+Worry (67.4 years; p=0.012). Proxies of AD patients with feelings of burden reported SCD (55.6%) significantly more frequently than proxies without feelings of burden (32.4%; p=0.025). Controls with AD Worry reported SCD+Worry (23.0%) significantly more frequently compared to controls without AD Worry (6.7%; p=0.021). In line with the latter result, there was a significant positive correlation between AD Worry and SCD+Worry (r=0.211, p=0.021) in the control sample. Conclusion: AD Worry is a widespread phenomenon within the examined cohorts of proxies of AD patients and controls. It is not associated with objective cognitive impairment. However, the higher presence of SCD+Worry in those controls who reported AD Worry and the higher presence of AD Worry among sons and daughters of AD patients compared to spouses indicate that AD Worry could be an early indicator of future cognitive impairment. Longitudinal studies examining larger samples are needed to further elucidate the potential association between AD Worry, SCD and future cognitive decline.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"54 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2017-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86517883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-02-01DOI: 10.4172/2161-0460.1000296
O. Kwon
Apolipoprotein E is a plasma protein that has an important role in transport and metabolism of lipids in serum as well as in central nervous system. Among the three common alleles, the e2 allele has the most stable structure followed by e3 and e4 in order. There is evidence for a deleterious role of apolipoprotein e4 by atherosclerosis and amyloid beta accumulation in brain and body by the differences of three-dimensional structures among the apoE isoforms. APOE e4 also seems to be related to cognitive decline in Parkinson’s disease but not too related to the age at onset of Parkinson’s disease.
{"title":"Is There Any Relationship between Apolipoprotein E Polymorphism andIdiopathic ParkinsonâÂÂs Disease?","authors":"O. Kwon","doi":"10.4172/2161-0460.1000296","DOIUrl":"https://doi.org/10.4172/2161-0460.1000296","url":null,"abstract":"Apolipoprotein E is a plasma protein that has an important role in transport and metabolism of lipids in serum as well as in central nervous system. Among the three common alleles, the e2 allele has the most stable structure followed by e3 and e4 in order. There is evidence for a deleterious role of apolipoprotein e4 by atherosclerosis and amyloid beta accumulation in brain and body by the differences of three-dimensional structures among the apoE isoforms. APOE e4 also seems to be related to cognitive decline in Parkinson’s disease but not too related to the age at onset of Parkinson’s disease.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"10 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2017-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72983512","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-01-20DOI: 10.4172/2161-0460.1000300
S. Choi, G. Ryu, D. H. Kim, D. Lee, Seunghoon Lee, S. Kim, K. H. Lee, Y. Woo, Yunhao Song, G. Im, T. Hu, Hong J Lee
Parkinson’s disease (PD), characterized by the loss of dopaminergic neurons in the substantia nigra, is one of the most common neurodegenerative disorders in elderly people. However, few effective therapies are available for neurodegenerative diseases, including PD. Stem cell therapies have been studied as potentially effective treatment options for neurodegenerative diseases through mechanisms of neuronal regeneration and substitution. Stem cells can migrate into injured regions and produce new neurons and glia, as well as neuroprotective molecules to improve neuron survival in the region. The survival and integration of these transplanted stem cells is an important issue for the success of stem cell therapy in neurodegenerative disease. Recent research in animals shows the promise of stem cell transplantation as a powerful treatment for Parkinson’s disease, among other neurodegenerative diseases, in the near future.
{"title":"Stem Cell Applications in Parkinsonâs Disease","authors":"S. Choi, G. Ryu, D. H. Kim, D. Lee, Seunghoon Lee, S. Kim, K. H. Lee, Y. Woo, Yunhao Song, G. Im, T. Hu, Hong J Lee","doi":"10.4172/2161-0460.1000300","DOIUrl":"https://doi.org/10.4172/2161-0460.1000300","url":null,"abstract":"Parkinson’s disease (PD), characterized by the loss of dopaminergic neurons in the substantia nigra, is one of the most common neurodegenerative disorders in elderly people. However, few effective therapies are available for neurodegenerative diseases, including PD. Stem cell therapies have been studied as potentially effective treatment options for neurodegenerative diseases through mechanisms of neuronal regeneration and substitution. Stem cells can migrate into injured regions and produce new neurons and glia, as well as neuroprotective molecules to improve neuron survival in the region. The survival and integration of these transplanted stem cells is an important issue for the success of stem cell therapy in neurodegenerative disease. Recent research in animals shows the promise of stem cell transplantation as a powerful treatment for Parkinson’s disease, among other neurodegenerative diseases, in the near future.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"29 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90801382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-01-16DOI: 10.4172/2161-0460.1000298
Jolanta Florczak Wyspianska, M. Owecki, M. Rzymkowska, H. Gabryel, W. Kozubski
Langerhans cell histiocytosis (LHC) is a rare proliferative disease of unknown etiology characterized by bone marrow-derived histiocyte-like cell proliferation. The disease is confirmed by electron microscopy or immunohistochemical reactivity of histiocytes to the CD1a receptor, langerin (CD207) and/or S100 protein. The clinical spectrum ranges from an acute disseminated disease to solitary or few chronic lesions of bone or other organs. Central nervous system invasion in LCH patients has rarely been reported, especially in the adult population. We report a case of an intracranial tumorous lesion as the first manifestation of LCH in a 23 year old Caucasian man. The patient presented a 2 year history of cognitive decline and a 7 year history of diabetes insipidus, diabetes mellitus, hypothyroidism and obesity. The histopathological findings of a lesion located in the hypothalamic region confirmed the diagnosis of LCH.
{"title":"Intracranial Tumorous Lesion as the First Manifestation of LangerhansCell Histiocytosis: A Diagnostic and Therapeutic Challenge - Case Report","authors":"Jolanta Florczak Wyspianska, M. Owecki, M. Rzymkowska, H. Gabryel, W. Kozubski","doi":"10.4172/2161-0460.1000298","DOIUrl":"https://doi.org/10.4172/2161-0460.1000298","url":null,"abstract":"Langerhans cell histiocytosis (LHC) is a rare proliferative disease of unknown etiology characterized by bone marrow-derived histiocyte-like cell proliferation. The disease is confirmed by electron microscopy or immunohistochemical reactivity of histiocytes to the CD1a receptor, langerin (CD207) and/or S100 protein. The clinical spectrum ranges from an acute disseminated disease to solitary or few chronic lesions of bone or other organs. Central nervous system invasion in LCH patients has rarely been reported, especially in the adult population. We report a case of an intracranial tumorous lesion as the first manifestation of LCH in a 23 year old Caucasian man. The patient presented a 2 year history of cognitive decline and a 7 year history of diabetes insipidus, diabetes mellitus, hypothyroidism and obesity. The histopathological findings of a lesion located in the hypothalamic region confirmed the diagnosis of LCH.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"8 1","pages":"1-5"},"PeriodicalIF":0.0,"publicationDate":"2017-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86046910","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2017-01-16DOI: 10.4172/2161-0460.1000299
P. Maiti, J. Rossignol, G. Dunbar
Accumulation of misfolded amyloid beta proteins (Aβ) and hyper phosphorylated-tau are the key players in the pathologenesis of Alzheimer’s disease (AD). Molecular chaperones (heat shock proteins, HSPs), autophagylysosomal pathways (ALPs), and chaperone-mediated autophagy (CMA) are actively involved in degradation of these aggregates. Dysregulation of these systems has been observed in the AD brain, which demands the maintenance or restoration of these systems. In this context, as an anti-amyloid, curcumin (Cur) has potential role for AD therapy. Becuase of its solubility and bioavailability issues, recently we have used solid lipid curucmin particles (SLCP), which showed great permeability and neuroprotection. In this context, the present study was designed to investigate the role of Cur on HSPs and ALPs, In vitro, after exposure to Aβ42. Human cortical neurons (SH-SY5Y) and mouse neuroblastoma (N2a) cells were exposed with Aβ42 (10 μM) for 24 h and incubated with or without different concentrations of dietary Cur and or SLCP and several markers for HSPs and ALPs were investigated. We found that the most HSPs (HSP90, HSP70, HSP60, HSP40) were downregulated after exposure to Aβ42 and Cur treatment restored their levels. Similarly, markers for CMA, such as HSC70, LAMP2A, CHIP were downregulated by the Aβ42 exposure and Cur and or SLCP treatment restored their levels. In contrast, macroautophagy markers, such as LC3A/B-II and beclin-1 were upregulated after exposure to Aβ42, while Cur and or SLCP treatment further increased their levels. Therefore, maintenance or restoration of HSPs and regulation of ALPs by Cur may provide a promising strategy to degrade Aβ-aggregates from neurons in the AD brain.
{"title":"Curcumin Modulates Molecular Chaperones and Autophagy-LysosomalPathways In Vitro after Exposure to Aò42","authors":"P. Maiti, J. Rossignol, G. Dunbar","doi":"10.4172/2161-0460.1000299","DOIUrl":"https://doi.org/10.4172/2161-0460.1000299","url":null,"abstract":"Accumulation of misfolded amyloid beta proteins (Aβ) and hyper phosphorylated-tau are the key players in the pathologenesis of Alzheimer’s disease (AD). Molecular chaperones (heat shock proteins, HSPs), autophagylysosomal pathways (ALPs), and chaperone-mediated autophagy (CMA) are actively involved in degradation of these aggregates. Dysregulation of these systems has been observed in the AD brain, which demands the maintenance or restoration of these systems. In this context, as an anti-amyloid, curcumin (Cur) has potential role for AD therapy. Becuase of its solubility and bioavailability issues, recently we have used solid lipid curucmin particles (SLCP), which showed great permeability and neuroprotection. In this context, the present study was designed to investigate the role of Cur on HSPs and ALPs, In vitro, after exposure to Aβ42. Human cortical neurons (SH-SY5Y) and mouse neuroblastoma (N2a) cells were exposed with Aβ42 (10 μM) for 24 h and incubated with or without different concentrations of dietary Cur and or SLCP and several markers for HSPs and ALPs were investigated. We found that the most HSPs (HSP90, HSP70, HSP60, HSP40) were downregulated after exposure to Aβ42 and Cur treatment restored their levels. Similarly, markers for CMA, such as HSC70, LAMP2A, CHIP were downregulated by the Aβ42 exposure and Cur and or SLCP treatment restored their levels. In contrast, macroautophagy markers, such as LC3A/B-II and beclin-1 were upregulated after exposure to Aβ42, while Cur and or SLCP treatment further increased their levels. Therefore, maintenance or restoration of HSPs and regulation of ALPs by Cur may provide a promising strategy to degrade Aβ-aggregates from neurons in the AD brain.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"16 1","pages":"1-12"},"PeriodicalIF":0.0,"publicationDate":"2017-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82660481","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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