Pub Date : 2017-07-10DOI: 10.4172/2161-0460.1000347
Daniela Fisichella
A sharp attention is devoted to mental health and mental illness by International Law and many International Organizations (IO’s) in XXI century. As a consequence of human rights huge extension, mental health is nowadays a target of international efforts striving to address both States national choices and international achievements. World Health Organization (WHO) is expressly engaged, but United Nations (UN) opened up the legal path in early nineties, by UN General Assembly (UNGA) 46/119 of 17 December 1991, The protection of persons with mental illness and the improvement of mental health care, where mental health care and facilities are pointed out; and if mental illness couldn’t be defined, Principle 4 (Determination of mental illness) of this Resolution is crucial to direct next improvements layout. From there, UN and WHO have been carrying on a unique approach to mental health, as proved by binding and non-binding international acts, surveys, guidelines – as the 2010 WHO mhGAP Intervention Guide, now updated in its 2016 version – adopted as a result of States consultation. UNGA Resolution 70/1 of 21 October 2015, Transforming Our World: the 2030 Agenda for Sustainable Development, envisaging 17 Sustainable Development Goals (and replacing past 8 Millennium Development Goals to be gained in 2015 at last) is the last step on the road of a global approach to health, both physical and mental in an holistic view of human beings. As stated in Declaration’s Introduction, “no one will be left behind”. This article aims to investigate mental health as an international legal issue on a broad sense, not only compared to lack of mental illness, but in a comprehensive view dealing with it by implementing International Law on Human Rights. Dementia prevention and care above other mental diseases is perceived in a global framework of domestic economic and social balance (2012 WHO Dementia, a Public Health Priority), even though national health care systems still depend upon national policies in investments assets. But States’ attitude to healthcare services in mental health should now be oriented by International Law current evolution.
{"title":"United Nations and World Health Organisation Engagement in TreatingGlobal Mental Health, with a Special Focus on Dementia","authors":"Daniela Fisichella","doi":"10.4172/2161-0460.1000347","DOIUrl":"https://doi.org/10.4172/2161-0460.1000347","url":null,"abstract":"A sharp attention is devoted to mental health and mental illness by International Law and many International Organizations (IO’s) in XXI century. As a consequence of human rights huge extension, mental health is nowadays a target of international efforts striving to address both States national choices and international achievements. World Health Organization (WHO) is expressly engaged, but United Nations (UN) opened up the legal path in early nineties, by UN General Assembly (UNGA) 46/119 of 17 December 1991, The protection of persons with mental illness and the improvement of mental health care, where mental health care and facilities are pointed out; and if mental illness couldn’t be defined, Principle 4 (Determination of mental illness) of this Resolution is crucial to direct next improvements layout. From there, UN and WHO have been carrying on a unique approach to mental health, as proved by binding and non-binding international acts, surveys, guidelines – as the 2010 WHO mhGAP Intervention Guide, now updated in its 2016 version – adopted as a result of States consultation. UNGA Resolution 70/1 of 21 October 2015, Transforming Our World: the 2030 Agenda for Sustainable Development, envisaging 17 Sustainable Development Goals (and replacing past 8 Millennium Development Goals to be gained in 2015 at last) is the last step on the road of a global approach to health, both physical and mental in an holistic view of human beings. As stated in Declaration’s Introduction, “no one will be left behind”. This article aims to investigate mental health as an international legal issue on a broad sense, not only compared to lack of mental illness, but in a comprehensive view dealing with it by implementing International Law on Human Rights. Dementia prevention and care above other mental diseases is perceived in a global framework of domestic economic and social balance (2012 WHO Dementia, a Public Health Priority), even though national health care systems still depend upon national policies in investments assets. But States’ attitude to healthcare services in mental health should now be oriented by International Law current evolution.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"49 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2017-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87028463","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 : 2017-07-07DOI: 10.4172/2161-0460.1000346
Huei-Yang Chen, P. Panegyres
In a recent report published by World Health Organisation, it was estimated that there were 46 million people living with dementia around the world and this number is projected to be tripled by 2050 [1]. With the increasing proportion of minorities among elderly populations [2] and a higher prevalence of dementia observed among Hispanics [3-5], Latinos [6] and African Americans [3-6], the burden of dementia in minorities is a challenge for many health systems. Being the most prevalent form of dementia and similar ethnic disparities were reported in Alzheimer’s disease (AD) [7], AD should be a priority for countries where populations are composed of a significant proportion of Hispanics and African Americans, like the United States.
{"title":"Ethnic Differences in Early Onset Alzheimer's Disease","authors":"Huei-Yang Chen, P. Panegyres","doi":"10.4172/2161-0460.1000346","DOIUrl":"https://doi.org/10.4172/2161-0460.1000346","url":null,"abstract":"In a recent report published by World Health Organisation, it was estimated that there were 46 million people living with dementia around the world and this number is projected to be tripled by 2050 [1]. With the increasing proportion of minorities among elderly populations [2] and a higher prevalence of dementia observed among Hispanics [3-5], Latinos [6] and African Americans [3-6], the burden of dementia in minorities is a challenge for many health systems. Being the most prevalent form of dementia and similar ethnic disparities were reported in Alzheimer’s disease (AD) [7], AD should be a priority for countries where populations are composed of a significant proportion of Hispanics and African Americans, like the United States.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"15 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2017-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74638468","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 : 2017-07-05DOI: 10.4172/2161-0460.1000342
Chun-Lin Lee, T. Pan
Alzheimer's disease (AD) and Parkinson’s disease (PD), which are senile neurodegenerative diseases, have become more common in recent year. An important cause for AD is currently the deposition of amyloid β (Aβ) in the brain, leading to severe oxidative stress and inflammation, as well as neuronal death and memory damage in AD patients. PD is a chronic degeneration of the central nervous system that mainly affects the motor system. Its symptoms usually appear gradually, and are most obviously tremors, body stiffness, slowed movement, and gait abnormality during early stage; though the mechanism for the death of dopaminergic neurons is not yet completely understood, oxidative stress has been shown to be a very important factor in triggering the development of PD in many human and animal studies. As has been revealed in past research, fermented products of Monascus and their extracts can effectively improve the course of AD and PD, possessing significant preventative and alleviating effects. The main effectors are confirmed to be monascin and ankaflavin for AD treatment, and dimerumic acid and deferricoprogen for PD treatment. This review, therefore, focuses on the analysis and comprehensive discussion of these four active components, for an overall understanding of their role in the AD and PD improvement function of Monascus fermented products.
{"title":"The Prevention of Alzheimer's Disease and ParkinsonâÂÂs Disease byMonascus purpureus NTU 568-Fermented Compounds","authors":"Chun-Lin Lee, T. Pan","doi":"10.4172/2161-0460.1000342","DOIUrl":"https://doi.org/10.4172/2161-0460.1000342","url":null,"abstract":"Alzheimer's disease (AD) and Parkinson’s disease (PD), which are senile neurodegenerative diseases, have become more common in recent year. An important cause for AD is currently the deposition of amyloid β (Aβ) in the brain, leading to severe oxidative stress and inflammation, as well as neuronal death and memory damage in AD patients. PD is a chronic degeneration of the central nervous system that mainly affects the motor system. Its symptoms usually appear gradually, and are most obviously tremors, body stiffness, slowed movement, and gait abnormality during early stage; though the mechanism for the death of dopaminergic neurons is not yet completely understood, oxidative stress has been shown to be a very important factor in triggering the development of PD in many human and animal studies. As has been revealed in past research, fermented products of Monascus and their extracts can effectively improve the course of AD and PD, possessing significant preventative and alleviating effects. The main effectors are confirmed to be monascin and ankaflavin for AD treatment, and dimerumic acid and deferricoprogen for PD treatment. This review, therefore, focuses on the analysis and comprehensive discussion of these four active components, for an overall understanding of their role in the AD and PD improvement function of Monascus fermented products.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"67 1","pages":"1-8"},"PeriodicalIF":0.0,"publicationDate":"2017-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77279013","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 : 2017-07-05DOI: 10.4172/2161-0460.1000344
Y. Kima, Jisu Parka, Yong-Keun Jung
Alzheimer’s disease (AD) is the most common and leading cause of dementia. AD has two different pathological hallmarks, extracellular amyloid beta plaques and intracellular neurofibrillary tangles (NFT). NFTs consist of abnormally modified tau protein that forms protein aggregates. Tau protein aggregates are prevalently observed as disease progresses and are believed to cause neuronal dysfunction. The caspase-3 cleaved form of tau, TauC3, is generated in cultured neurons under stress and is found in the brains of patients with AD in the early stages of disease when patients are asymptomatic. TauC3 accelerates tau oligomerization in vitro and in vivo, and induces neuronal degeneration. Moreover, the neuronal expression of TauC3 in transgenic mice causes memory deficits at a young age, which is concomitant with the appearance of tau oligomers. The removal of TauC3-containing oligomers and aggregates using drug treatment improves both memory and synaptic function. These findings demonstrate that TauC3 is critical for the formation of tau oligomers and small aggregates and may ultimately play a role in the rapid memory impairments observed in AD. Overall, TauC3 may represent a new therapeutic target for the prevention of AD.
{"title":"New Insight into Alzheimer's Disease via Caspase 3-cleaved Tau: Pathogenic Role in Tau Oligomer Formation and Memory Deficits","authors":"Y. Kima, Jisu Parka, Yong-Keun Jung","doi":"10.4172/2161-0460.1000344","DOIUrl":"https://doi.org/10.4172/2161-0460.1000344","url":null,"abstract":"Alzheimer’s disease (AD) is the most common and leading cause of dementia. AD has two different pathological hallmarks, extracellular amyloid beta plaques and intracellular neurofibrillary tangles (NFT). NFTs consist of abnormally modified tau protein that forms protein aggregates. Tau protein aggregates are prevalently observed as disease progresses and are believed to cause neuronal dysfunction. The caspase-3 cleaved form of tau, TauC3, is generated in cultured neurons under stress and is found in the brains of patients with AD in the early stages of disease when patients are asymptomatic. TauC3 accelerates tau oligomerization in vitro and in vivo, and induces neuronal degeneration. Moreover, the neuronal expression of TauC3 in transgenic mice causes memory deficits at a young age, which is concomitant with the appearance of tau oligomers. The removal of TauC3-containing oligomers and aggregates using drug treatment improves both memory and synaptic function. These findings demonstrate that TauC3 is critical for the formation of tau oligomers and small aggregates and may ultimately play a role in the rapid memory impairments observed in AD. Overall, TauC3 may represent a new therapeutic target for the prevention of AD.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"90 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2017-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85644657","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 : 2017-07-05DOI: 10.4172/2161-0460.1000345
Zhiqian Tong
Given the dramatic increase in Alzheimer’s disease (AD) cases globally, the identification of a suitable biomarker in easily collectable samples (e.g. plasma, blood, saliva and urine) for diagnosing AD is therefore of utmost importance. Previous studies indicated that excess formaldehyde contributes to Aβ aggregation and Tau hyper phosphorylation, both phenomena directly linked to the progress of AD. Our 7 year’s cross-sectional survey showed that morning urine formaldehyde levels were correlated positively with the severe degree of sporadic dementia, suggesting that urine formaldehyde measurement most likely acts as a suitable non-invasive method to support diagnostic purposes. In this a short review article, we provide a short overview of the animal and clinical studies on the possible mechanisms of exogenous and endogenous factors cause formaldehyde accumulation, which plays a critical role in the pathogenesis of both genetic dementia and sporadic dementia. Urine formaldehyde will be of significant value for the non-invasive diagnosis of cognitive ability in AD, but the more sensitive method for detecting formaldehyde concentrations and a longitudinal (long-term follow-up) study would be required to prove conclusively such a relationship between urine formaldehyde and dementia.
{"title":"Urine Formaldehyde: A Non-Invasive Marker for AlzheimerâÂÂs Disease?","authors":"Zhiqian Tong","doi":"10.4172/2161-0460.1000345","DOIUrl":"https://doi.org/10.4172/2161-0460.1000345","url":null,"abstract":"Given the dramatic increase in Alzheimer’s disease (AD) cases globally, the identification of a suitable biomarker in easily collectable samples (e.g. plasma, blood, saliva and urine) for diagnosing AD is therefore of utmost importance. Previous studies indicated that excess formaldehyde contributes to Aβ aggregation and Tau hyper phosphorylation, both phenomena directly linked to the progress of AD. Our 7 year’s cross-sectional survey showed that morning urine formaldehyde levels were correlated positively with the severe degree of sporadic dementia, suggesting that urine formaldehyde measurement most likely acts as a suitable non-invasive method to support diagnostic purposes. In this a short review article, we provide a short overview of the animal and clinical studies on the possible mechanisms of exogenous and endogenous factors cause formaldehyde accumulation, which plays a critical role in the pathogenesis of both genetic dementia and sporadic dementia. Urine formaldehyde will be of significant value for the non-invasive diagnosis of cognitive ability in AD, but the more sensitive method for detecting formaldehyde concentrations and a longitudinal (long-term follow-up) study would be required to prove conclusively such a relationship between urine formaldehyde and dementia.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"13 1","pages":"1-5"},"PeriodicalIF":0.0,"publicationDate":"2017-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90691213","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 : 2017-06-27DOI: 10.4172/2161-0460.1000341
N. Origlia, L. Domenici
Alzheimer’s disease (AD) is a multifactorial neurodegenerative disease, primarily affecting the elderly. Pathophysiological mechanisms have been elucidated in the past decades. First of all, AD is progressive leading to cognitive deficits till dementia. Pathologically, AD features synaptic dysfunction with changes of neuronal circuitry, progressive accumulation of protein aggregates such as the beta amyloid and tau. Herein we critically review neurobiological processes and factors involved in AD, in light of recent results on synaptic dysfunction and impairment of neuronal activity.
{"title":"Synaptic Function and Dysfunction in AlzheimerâÂÂs Disease","authors":"N. Origlia, L. Domenici","doi":"10.4172/2161-0460.1000341","DOIUrl":"https://doi.org/10.4172/2161-0460.1000341","url":null,"abstract":"Alzheimer’s disease (AD) is a multifactorial neurodegenerative disease, primarily affecting the elderly. Pathophysiological mechanisms have been elucidated in the past decades. First of all, AD is progressive leading to cognitive deficits till dementia. Pathologically, AD features synaptic dysfunction with changes of neuronal circuitry, progressive accumulation of protein aggregates such as the beta amyloid and tau. Herein we critically review neurobiological processes and factors involved in AD, in light of recent results on synaptic dysfunction and impairment of neuronal activity.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"19 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2017-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85336142","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 : 2017-06-21DOI: 10.4172/2161-0460.1000338
P. Grant, M. Bhaskar, B. Binukumar, H. Pant
Neurodegenerative disorders such as Alzheimer’s or Parkinson’s are diseases of aging. Mutations, lesions, neuronal insults, the genetic and stochastic “slings and arrows” of living, accumulate and downgrade organ function. Microarray analyses of aging brain identify patterns of genetic changes that correlate with neurodegenerative phenotypes. Genes involved in synaptic transmission, mitochondrial function and protein turnover are downregulated while significant numbers of genes regulating DNA repair, stress responses and inflammation are upregulated. This impact on the brain induces, a complex, multidimensional network of abnormal interactions leading to deposits of protein aggregates such as amyloid plaques, tau and neurofilament proteins tangles. For some, this pathology leads to neuron loss, behavioral defects, cognitive decline and death. Therapeutic approaches for AD, for example, target the molecular pathways leading to plaques and tangles; these include kinases and phosphatases. Among kinases, one stands out, Cdk5/p35, essential for neuronal migration, synapse formation, function and survival. Studies have shown that aging-induced neuronal stress deregulates and hyper activates Cdk5, a ubiquitous feature of neuronal disorders such as Alzheimer’s, Amyotropic lateral sclerosis (ALS) and Parkinson’s (PD). Among its many effects, hyperactive Cdk5 is implicated in the production of abnormal phosphorylated protein aggregates and is a therapeutic target. Roscovitine and related compounds inhibit Cdk5 activity but not specifically; cell cycle Cdks and other kinases are equally affected. In our laboratory two truncated peptides CIP (126a.a) and P5 (24a.a.), derived from p35, activator, of Cdk5 have been shown to specifically inhibit hyperactive Cdk5 in vitro, in cortical neurons and in AD, ALS and PD model mice. As a result the neurodegenerative phenotype was diminished; aggregates and inflammation were reduced, abnormal behavior was improved and increased animal’s longevity. We believe these peptides are excellent therapeutic candidates for those neurodegenerative disorders expressing hyperactive Cdk5 in the brain.
{"title":"Peptides Derived from Neuronal Cell Cycle like Kinase 5 Activator p35, inNeurodegeneration; Pathology and Therapy","authors":"P. Grant, M. Bhaskar, B. Binukumar, H. Pant","doi":"10.4172/2161-0460.1000338","DOIUrl":"https://doi.org/10.4172/2161-0460.1000338","url":null,"abstract":"Neurodegenerative disorders such as Alzheimer’s or Parkinson’s are diseases of aging. Mutations, lesions, neuronal insults, the genetic and stochastic “slings and arrows” of living, accumulate and downgrade organ function. Microarray analyses of aging brain identify patterns of genetic changes that correlate with neurodegenerative phenotypes. Genes involved in synaptic transmission, mitochondrial function and protein turnover are downregulated while significant numbers of genes regulating DNA repair, stress responses and inflammation are upregulated. This impact on the brain induces, a complex, multidimensional network of abnormal interactions leading to deposits of protein aggregates such as amyloid plaques, tau and neurofilament proteins tangles. For some, this pathology leads to neuron loss, behavioral defects, cognitive decline and death. Therapeutic approaches for AD, for example, target the molecular pathways leading to plaques and tangles; these include kinases and phosphatases. Among kinases, one stands out, Cdk5/p35, essential for neuronal migration, synapse formation, function and survival. Studies have shown that aging-induced neuronal stress deregulates and hyper activates Cdk5, a ubiquitous feature of neuronal disorders such as Alzheimer’s, Amyotropic lateral sclerosis (ALS) and Parkinson’s (PD). Among its many effects, hyperactive Cdk5 is implicated in the production of abnormal phosphorylated protein aggregates and is a therapeutic target. Roscovitine and related compounds inhibit Cdk5 activity but not specifically; cell cycle Cdks and other kinases are equally affected. In our laboratory two truncated peptides CIP (126a.a) and P5 (24a.a.), derived from p35, activator, of Cdk5 have been shown to specifically inhibit hyperactive Cdk5 in vitro, in cortical neurons and in AD, ALS and PD model mice. As a result the neurodegenerative phenotype was diminished; aggregates and inflammation were reduced, abnormal behavior was improved and increased animal’s longevity. We believe these peptides are excellent therapeutic candidates for those neurodegenerative disorders expressing hyperactive Cdk5 in the brain.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"1 1","pages":"1-8"},"PeriodicalIF":0.0,"publicationDate":"2017-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84073408","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 : 2017-06-21DOI: 10.4172/2161-0460.1000339
Feixiang Wang, Yali Jia, Jiajing Liu, Jinglei Zhai, N. Cao, W. Yue, Huixia He, X. Pei
Objective: Alzheimer's disease (AD) is a chronic neurodegenerative disease with multiple etiological factors, characterized by neurofibrillary tangles of hyperphosphorylated tau (pTau) protein. Periodontal ligament stem cells (PDLSCs) have been utilized to reconstruct tissues destroyed by chronic pathology, but the use of PDLSCs for treating AD remains unstudied. Methods: We investigated the in vitro effects of PDLSCs on the function of SH-SY5Y cells that had been established as models of AD via use of okadaic acid (OA). To this end, we utilized immunofluorescence, CCK-8 assay, flow cytometry, western blot, and confocal and transmission electron microscopy. Results: Co-culturing OA-treated SH-SY5Y cells with PDLSCs for 24 h was associated with improved cell shape, dendrites, cytoskeleton structure, and cell viability relative to the model without PDLSCs, while cell apoptosis and pTau protein levels were lower. Conclusion: These findings suggest that treatment of AD-model cells with PDLSCs promoted the recovery of cell shape, structure, and function. PDLSCs may be a novel research target for clinical treatment of patients with AD. Further investigations of the effect of PDLSCs in AD from the behavioral or molecular levels are warranted.
{"title":"Beneficial Effects of Periodontal Ligament Stem Cells in Alzheimer'sDisease Cell Model","authors":"Feixiang Wang, Yali Jia, Jiajing Liu, Jinglei Zhai, N. Cao, W. Yue, Huixia He, X. Pei","doi":"10.4172/2161-0460.1000339","DOIUrl":"https://doi.org/10.4172/2161-0460.1000339","url":null,"abstract":"Objective: Alzheimer's disease (AD) is a chronic neurodegenerative disease with multiple etiological factors, characterized by neurofibrillary tangles of hyperphosphorylated tau (pTau) protein. Periodontal ligament stem cells (PDLSCs) have been utilized to reconstruct tissues destroyed by chronic pathology, but the use of PDLSCs for treating AD remains unstudied. \u0000Methods: We investigated the in vitro effects of PDLSCs on the function of SH-SY5Y cells that had been established as models of AD via use of okadaic acid (OA). To this end, we utilized immunofluorescence, CCK-8 assay, flow cytometry, western blot, and confocal and transmission electron microscopy. \u0000Results: Co-culturing OA-treated SH-SY5Y cells with PDLSCs for 24 h was associated with improved cell shape, dendrites, cytoskeleton structure, and cell viability relative to the model without PDLSCs, while cell apoptosis and pTau protein levels were lower. \u0000Conclusion: These findings suggest that treatment of AD-model cells with PDLSCs promoted the recovery of cell shape, structure, and function. PDLSCs may be a novel research target for clinical treatment of patients with AD. Further investigations of the effect of PDLSCs in AD from the behavioral or molecular levels are warranted.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"324 1","pages":"1-8"},"PeriodicalIF":0.0,"publicationDate":"2017-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82919808","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 : 2017-06-20DOI: 10.4172/2161-0460.1000336
A. Ojeda, H. R. Martinez, F. G. Rivera, J. Garza, Hector Canfield Medina, S. Davila
Background: Abnormalities in cerebral vasomotor reactivity (CVR) in patients with idiopathic Parkinson’s disease (IPD) have not been well determined; nonetheless, a vascular mechanism may be involved in some patients with this neurodegenerative disorder. The objective of this study was to compare CVR in IPD patients and subjects without Parkinson’s disease. Methods: A cross-sectional pilot study was conducted including Hispanic IPD patients and a control group. CVR in the middle cerebral arteries (MCA) was measured by transcranial Doppler ultrasonography (TCD) at rest and after inhalation of 7% CO2. A comparison of CVR in the MCA of both groups was performed. Results: 27 IPD Hispanic patients with a recent brain MRI were evaluated. The CVR showed a significant difference between the two groups (p=0.044). The CVR in 70% of the IPD patients was low in comparison to control subjects. Conclusion: IPD patients are prone to exhibit diminished CVR in comparison with control group. Further studies may demonstrate this tendency and its implication in disease severity.
{"title":"Cerebral Vasoreactivity in Parkinson's Disease: A Cross-Sectional Pilot Study in a Hispanic Cohort","authors":"A. Ojeda, H. R. Martinez, F. G. Rivera, J. Garza, Hector Canfield Medina, S. Davila","doi":"10.4172/2161-0460.1000336","DOIUrl":"https://doi.org/10.4172/2161-0460.1000336","url":null,"abstract":"Background: Abnormalities in cerebral vasomotor reactivity (CVR) in patients with idiopathic Parkinson’s disease (IPD) have not been well determined; nonetheless, a vascular mechanism may be involved in some patients with this neurodegenerative disorder. The objective of this study was to compare CVR in IPD patients and subjects without Parkinson’s disease. Methods: A cross-sectional pilot study was conducted including Hispanic IPD patients and a control group. CVR in the middle cerebral arteries (MCA) was measured by transcranial Doppler ultrasonography (TCD) at rest and after inhalation of 7% CO2. A comparison of CVR in the MCA of both groups was performed. Results: 27 IPD Hispanic patients with a recent brain MRI were evaluated. The CVR showed a significant difference between the two groups (p=0.044). The CVR in 70% of the IPD patients was low in comparison to control subjects. Conclusion: IPD patients are prone to exhibit diminished CVR in comparison with control group. Further studies may demonstrate this tendency and its implication in disease severity.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"1 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2017-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85915014","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}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：