Pub Date : 2018-01-01DOI: 10.4172/2161-0460.1000413
H. Sawada, T. Oeda, A. Umemura, T. Satoshi, M. Kohsaka, Kwiyoung Park, K. Yamamoto
Psychosis is a common non-motor complication in Parkinson disease, and affects the quality of life of patients and their care-givers. This psychosis is caused by intrinsic (pathological and genetic) and extrinsic factors. Pathological factors include the severity of Lewy body pathology, degeneration of cholinergic neurons and overstimulation of serotonin receptors. Genetic factors include apolipoprotein e4, cholecystokinin genotyping, and glucocerebrosidase mutations. Extrinsic factors that trigger psychosis include systemic inflammation and medication of risky drugs. To prevent such psychosis, it is important to examine systemic infection, cease high-risk drugs, and then consider prescription of anti-psychotic drugs. This review is to discuss pathogenesis and therapeutic strategy of psychosis in Parkinson disease.
{"title":"Risks and Triggers of Psychosis in Parkinson Disease","authors":"H. Sawada, T. Oeda, A. Umemura, T. Satoshi, M. Kohsaka, Kwiyoung Park, K. Yamamoto","doi":"10.4172/2161-0460.1000413","DOIUrl":"https://doi.org/10.4172/2161-0460.1000413","url":null,"abstract":"Psychosis is a common non-motor complication in Parkinson disease, and affects the quality of life of patients and their care-givers. This psychosis is caused by intrinsic (pathological and genetic) and extrinsic factors. Pathological factors include the severity of Lewy body pathology, degeneration of cholinergic neurons and overstimulation of serotonin receptors. Genetic factors include apolipoprotein e4, cholecystokinin genotyping, and glucocerebrosidase mutations. Extrinsic factors that trigger psychosis include systemic inflammation and medication of risky drugs. To prevent such psychosis, it is important to examine systemic infection, cease high-risk drugs, and then consider prescription of anti-psychotic drugs. This review is to discuss pathogenesis and therapeutic strategy of psychosis in Parkinson disease.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"12 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84987028","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 : 2018-01-01DOI: 10.4172/2161-0460.1000419
T. Fujino, Tatsuo Yamada, T. Asada, M. Ichimaru, Y. Tsuboi, C. Wakana, S. Mawatari
Objective: It has been shown that plasmalogens (Pls) in the brain tissue and blood decrease among Alzheimer’s disease (AD) patients. We first confirmed the effects of Pls on animal AD models, and subsequently reported that the ingestion of 1 mg Pls was effective for AD patients in a randomized, placebo-controlled trial with mild cognitive impairment (MCI) or mild AD patients. The present study examined the efficacy of orally administered Pls on patients with MCI enrolled in the previous trial in terms of individual domains of the Mini Mental State Examination-Japanese (MMSE-J). Methods: The present analysis used 178 patients with MCI out of the 276 patients with either MCI or AD in the previously reported trial, and assessed the 24 week change in the domain-specific scores of the MMSE-J. Originally, the randomized, placebo-controlled trial was performed for 276 patients at age of 60-85 years who had the MMSE-J score of 20-27 points and the Geriatric Depression Scale-Short Version-Japanese Version (GDS-S-J) score of 5 points or less. The patients were randomly allocated to either a treatment with 1 mg of scallop-derived Pls daily or a placebo treatment. The primary outcome was a 24 week change in the MMSE-J. The registered number of the trial is UMIN000014945. Results: The MMSE-J total score improved statistically significantly in the Pls treatment but not in the placebo treatment, resulting in no significant between-treatment difference. With respect to one of the MMSE-J domains, orientation to place, the Pls treatment showed a significant improvement and the placebo treatment showed no such improvement; the between-treatment difference was statistically significant (p=0.003). The domain for orientation to time worsened significantly at endpoint in the placebo treatment, while the Pls treatment showed no worsening. However, the between-treatment difference failed to reach the statistical significance. No significant change was found in either treatment regarding the other MMSE-J domains. Conclusion: These findings suggest that oral administration of 1 mg Pls enhances cognitive function of MCI patients, especially orientation to place.
{"title":"Effects of Plasmalogen on Patients with Mild Cognitive Impairment: A Randomized, Placebo-Controlled Trial in Japan","authors":"T. Fujino, Tatsuo Yamada, T. Asada, M. Ichimaru, Y. Tsuboi, C. Wakana, S. Mawatari","doi":"10.4172/2161-0460.1000419","DOIUrl":"https://doi.org/10.4172/2161-0460.1000419","url":null,"abstract":"Objective: It has been shown that plasmalogens (Pls) in the brain tissue and blood decrease among Alzheimer’s disease (AD) patients. We first confirmed the effects of Pls on animal AD models, and subsequently reported that the ingestion of 1 mg Pls was effective for AD patients in a randomized, placebo-controlled trial with mild cognitive impairment (MCI) or mild AD patients. The present study examined the efficacy of orally administered Pls on patients with MCI enrolled in the previous trial in terms of individual domains of the Mini Mental State Examination-Japanese (MMSE-J). Methods: The present analysis used 178 patients with MCI out of the 276 patients with either MCI or AD in the previously reported trial, and assessed the 24 week change in the domain-specific scores of the MMSE-J. Originally, the randomized, placebo-controlled trial was performed for 276 patients at age of 60-85 years who had the MMSE-J score of 20-27 points and the Geriatric Depression Scale-Short Version-Japanese Version (GDS-S-J) score of 5 points or less. The patients were randomly allocated to either a treatment with 1 mg of scallop-derived Pls daily or a placebo treatment. The primary outcome was a 24 week change in the MMSE-J. The registered number of the trial is UMIN000014945. Results: The MMSE-J total score improved statistically significantly in the Pls treatment but not in the placebo treatment, resulting in no significant between-treatment difference. With respect to one of the MMSE-J domains, orientation to place, the Pls treatment showed a significant improvement and the placebo treatment showed no such improvement; the between-treatment difference was statistically significant (p=0.003). The domain for orientation to time worsened significantly at endpoint in the placebo treatment, while the Pls treatment showed no worsening. However, the between-treatment difference failed to reach the statistical significance. No significant change was found in either treatment regarding the other MMSE-J domains. Conclusion: These findings suggest that oral administration of 1 mg Pls enhances cognitive function of MCI patients, especially orientation to place.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"3 1","pages":"1-5"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85286592","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 : 2018-01-01DOI: 10.4172/2161-0460.1000440
K. Kanaya, S. Abe, H. Hanyu
To clarify differences between dementia with Lewy Bodies (DLB) and Alzheimer’s disease (AD) in the actual clinical setting, we studied sites of decreased cerebral blood flow (CBF) in cases of DLB and AD by 99mT-ECD-SPECT imaging using statistical parametric mapping (SPM8). In addition, the drug sensitivity was analyzed by SPM8. Twentyfive cases were classified as DLB with AD (DLB-w) and 8 cases were DLB without AD (DLB-wo). Sites of decreased CBF in the DLB-w group were observed in the posterior cingulate gyrus, bilateral parietotemporal association areas and the occipital lobe, and these sites resembled the pattern of decreased CBF associated with AD. Among the DLBwo cases, decreased CBF was observed in frontal lobe, anterior cingulate gyrus and occipital lobe. In a comparison of sites of decreased CBF prior to treatment between 15 cases in the group exhibiting drug sensitivity and 18 cases in the group not exhibiting drug sensitivity, the drug sensitivity group exhibited more prominent decreases in CBF in the frontal lobe. In summary, 78% of DLB cases were determined to be complicated with DAT based on SPECT imaging, and the pattern of decreased CBF in these cases resembled that of DAT.
{"title":"Evaluation of Cerebral Blood Flow in Dementia with Lewy Bodies by 99mTECD SPECT Imaging","authors":"K. Kanaya, S. Abe, H. Hanyu","doi":"10.4172/2161-0460.1000440","DOIUrl":"https://doi.org/10.4172/2161-0460.1000440","url":null,"abstract":"To clarify differences between dementia with Lewy Bodies (DLB) and Alzheimer’s disease (AD) in the actual clinical setting, we studied sites of decreased cerebral blood flow (CBF) in cases of DLB and AD by 99mT-ECD-SPECT imaging using statistical parametric mapping (SPM8). In addition, the drug sensitivity was analyzed by SPM8. Twentyfive cases were classified as DLB with AD (DLB-w) and 8 cases were DLB without AD (DLB-wo). Sites of decreased CBF in the DLB-w group were observed in the posterior cingulate gyrus, bilateral parietotemporal association areas and the occipital lobe, and these sites resembled the pattern of decreased CBF associated with AD. Among the DLBwo cases, decreased CBF was observed in frontal lobe, anterior cingulate gyrus and occipital lobe. In a comparison of sites of decreased CBF prior to treatment between 15 cases in the group exhibiting drug sensitivity and 18 cases in the group not exhibiting drug sensitivity, the drug sensitivity group exhibited more prominent decreases in CBF in the frontal lobe. In summary, 78% of DLB cases were determined to be complicated with DAT based on SPECT imaging, and the pattern of decreased CBF in these cases resembled that of DAT.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"2 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73301467","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 : 2018-01-01DOI: 10.4172/2161-0460.1000438
M. Chataigner, A. Dinel, V. Pallet, S. Layé, C. Joffre
Aging is associated to cognitive decline that can lead to neurodegenerative diseases and constitutes one of the main social and economic issues of the 21st century. The loss of memory, orientation and processing abilities associated with aging are involved in the loss of autonomy and in the decline in the quality of life in the elderly. Brain structures involved in memory such as hippocampus, cortex and striatum, are particularly affected by molecular and cellular damage during this period. Lipid metabolism and neurofunctional alterations, including disturbances in synaptic plasticity and neurogenesis, chronic low-grade inflammation and increased oxidative stress, are partly to be involved in age-related cognitive decline. Actually, nutrition represents a strategy of choice to prevent or delay these impairments since many studies have provided valuable data concerning the effect of dietary patterns and specific nutrients on cognitive function. From all nutrients, some of them are particularly attractive. Indeed, n-3 polyunsaturated acids (PUFAs), especially docosahexaenoic acid (DHA), have been identified for their beneficial effects on cognition, notably by acting on brain plasticity (synaptic plasticity, neurogenesis), neuroinflammation and oxidative stress. Other nutrients such as vitamin A, vitamin E, vitamin D, polyphenols as well as pre- and probiotics have aroused a growing interest in decreasing cognitive disorders. As nutrition has to be taken as a whole, we first described the effects of the Mediterranean diet which constitutes the most complete association of nutrients and (DHA from fish, vitamins and polyphenols from fruits and vegetables) represents a global vision of nutrition, then we focused on the interest of combining DHA and micronutrients contained in this diet as well as pre- and probiotics, to prevent age-related cognitive decline and reported the synergistic effects of these associations. Finally, we completed with benefits from dairy products that increase DHA incorporation.
{"title":"The Interest of Adding Micronutrients to Docosahexaenoic Acid Supplementation to Prevent Age-Related Cognitive Decline","authors":"M. Chataigner, A. Dinel, V. Pallet, S. Layé, C. Joffre","doi":"10.4172/2161-0460.1000438","DOIUrl":"https://doi.org/10.4172/2161-0460.1000438","url":null,"abstract":"Aging is associated to cognitive decline that can lead to neurodegenerative diseases and constitutes one of the main social and economic issues of the 21st century. The loss of memory, orientation and processing abilities associated with aging are involved in the loss of autonomy and in the decline in the quality of life in the elderly. Brain structures involved in memory such as hippocampus, cortex and striatum, are particularly affected by molecular and cellular damage during this period. Lipid metabolism and neurofunctional alterations, including disturbances in synaptic plasticity and neurogenesis, chronic low-grade inflammation and increased oxidative stress, are partly to be involved in age-related cognitive decline. Actually, nutrition represents a strategy of choice to prevent or delay these impairments since many studies have provided valuable data concerning the effect of dietary patterns and specific nutrients on cognitive function. From all nutrients, some of them are particularly attractive. Indeed, n-3 polyunsaturated acids (PUFAs), especially docosahexaenoic acid (DHA), have been identified for their beneficial effects on cognition, notably by acting on brain plasticity (synaptic plasticity, neurogenesis), neuroinflammation and oxidative stress. Other nutrients such as vitamin A, vitamin E, vitamin D, polyphenols as well as pre- and probiotics have aroused a growing interest in decreasing cognitive disorders. As nutrition has to be taken as a whole, we first described the effects of the Mediterranean diet which constitutes the most complete association of nutrients and (DHA from fish, vitamins and polyphenols from fruits and vegetables) represents a global vision of nutrition, then we focused on the interest of combining DHA and micronutrients contained in this diet as well as pre- and probiotics, to prevent age-related cognitive decline and reported the synergistic effects of these associations. Finally, we completed with benefits from dairy products that increase DHA incorporation.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"27 1","pages":"1-15"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72895431","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 : 2018-01-01DOI: 10.4172/2161-0460.1000436
R. Romero, E. Salazar-Alcalá, N. Cedeno, M. Fernandez-Mestre
Objective: Based on that the association of the e4 allele of the APOE gene with the development of late-onset AD is one of the strongest and that TLR4 has been involved in AD pathogenesis. The aim of the present work was to study the role of rs4986791 polymorphism of the TLR4 gene in the development of AD and correlate any such association with the presence of allele e4 of the APOE gene. Methods: We included 161 unrelated Venezuelan subjects classified as either AD patients (n=61) or healthy individuals (n=100). Polymorphisms of TLR4 and APOE genes were identified with PCR-SSP and PCR-RFLP, respectively. Results: The rs4986791 polymorphism does not appear to be related to AD, although the presence of the CC genotype and the C allele apparently confers three times higher risk of developing AD. Finally, positive and negative associations among the combinations TLR4 /APOE genes and AD were observed. Conclusion: The results suggest the absence of any association between rs4986791 polymorphism of TLR4 gene and susceptibility to AD and the association of the e4 allele of the APOE gene with the development of this pathology was confirmed.
{"title":"Role of the TLR4 rs4986791 Polymorphism in the Development of Lateonset Alzheimer Disease and its Relationship with APOE*4","authors":"R. Romero, E. Salazar-Alcalá, N. Cedeno, M. Fernandez-Mestre","doi":"10.4172/2161-0460.1000436","DOIUrl":"https://doi.org/10.4172/2161-0460.1000436","url":null,"abstract":"Objective: Based on that the association of the e4 allele of the APOE gene with the development of late-onset AD is one of the strongest and that TLR4 has been involved in AD pathogenesis. The aim of the present work was to study the role of rs4986791 polymorphism of the TLR4 gene in the development of AD and correlate any such association with the presence of allele e4 of the APOE gene. Methods: We included 161 unrelated Venezuelan subjects classified as either AD patients (n=61) or healthy individuals (n=100). Polymorphisms of TLR4 and APOE genes were identified with PCR-SSP and PCR-RFLP, respectively. Results: The rs4986791 polymorphism does not appear to be related to AD, although the presence of the CC genotype and the C allele apparently confers three times higher risk of developing AD. Finally, positive and negative associations among the combinations TLR4 /APOE genes and AD were observed. Conclusion: The results suggest the absence of any association between rs4986791 polymorphism of TLR4 gene and susceptibility to AD and the association of the e4 allele of the APOE gene with the development of this pathology was confirmed.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"19 1","pages":"1-5"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86022074","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 : 2018-01-01DOI: 10.4172/2161-0460.1000418
F. Tang
radiation suggested that ionizing radiation was a risk factor for AD. Intranasal inhalation of radon gas could subject the rhinencephalon and hippocampus to damaging radiation that initiated AD [8]. The Alzheimer neurofibrillary tangle is composed of tau, which is one of the most common pathological hallmarks of AD and tau aggregation pathology at Braak stage 1 1 (out of 6 Braak stages) or beyond affects 50% of the population over the age of 45 [9-11]. Our recent review of the effect of the preand post-natal irradiation on animal models and human studies indicated many similarities in hippocampal neuropathology, cognitive impairment and relevant molecular mechanisms between Alzheimer’s disease and early life radiation exposure-induced neuropsychological disorders [12-16]. It suggests that irradiation of the brain in early human life may set abnormal developmental events into motion that starts from tau aggregation at the ages of 40s and 50s, leading to the development of Alzheimer’s Disease at the late stages of human life. At molecular level, preor post-natal irradiation induced brain oxidative stress [15], neuroinflammatory response [16,17], capillary loss or impairment of
{"title":"Radiation and Alzheimer's Disease (AD)","authors":"F. Tang","doi":"10.4172/2161-0460.1000418","DOIUrl":"https://doi.org/10.4172/2161-0460.1000418","url":null,"abstract":"radiation suggested that ionizing radiation was a risk factor for AD. Intranasal inhalation of radon gas could subject the rhinencephalon and hippocampus to damaging radiation that initiated AD [8]. The Alzheimer neurofibrillary tangle is composed of tau, which is one of the most common pathological hallmarks of AD and tau aggregation pathology at Braak stage 1 1 (out of 6 Braak stages) or beyond affects 50% of the population over the age of 45 [9-11]. Our recent review of the effect of the preand post-natal irradiation on animal models and human studies indicated many similarities in hippocampal neuropathology, cognitive impairment and relevant molecular mechanisms between Alzheimer’s disease and early life radiation exposure-induced neuropsychological disorders [12-16]. It suggests that irradiation of the brain in early human life may set abnormal developmental events into motion that starts from tau aggregation at the ages of 40s and 50s, leading to the development of Alzheimer’s Disease at the late stages of human life. At molecular level, preor post-natal irradiation induced brain oxidative stress [15], neuroinflammatory response [16,17], capillary loss or impairment of","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"67 1","pages":"1-2"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80259403","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 : 2018-01-01DOI: 10.4172/2161-0460.1000423
A. Gunten, Marie-Thérèse Clerc, R. Tomar, P. John-Smith
Increasingly people are surviving into old age both in high and middle/low income countries. The increase in longevity is associated with increased levels of morbidity of both somatic and mental disorders during those added years. These pathologies prompt developing strategies for effective prediction, prevention and treatment of such disorders, among them the dementias such as Alzheimer’s disease (AD). Aging lies on a temporal continuum that starts at conception and ends at death. It refers to the aging processes occurring during an individual’s lifetime. However, our understanding of aging remains limited. In the early stages of dementia, distinguishing normal from pathological aging remains complex. Medical research customarily investigates the immediate mechanisms or pathogenesis of “how” diseases come about and affect patients. Evolutionary perspectives consider the reasons “why” people may have become particularly vulnerable to different conditions. Examining why people age is illuminating. Around the question whether aging is adaptive, we consider some evolutionary concepts useful around aging theories, among others antagonistic pleiotropy and life history theory and more recent concepts including evolvability and evolutionary developmental biology. As AD seems to be specific to homo sapiens, its existence may in part be anchored in the adaptive changes that have occurred after the hominidae separated from the pongidae. Around the question why apparently non-adaptive conditions such as AD are so frequent, we consider, among other aspects, brain development including the related phenomena of altriciality and grandmothering, the evolution of ApoE and the genome lag hypothesis. We consider the idea that the neuropathological hallmarks of AD help mitigate neurodegeneration and cognitive decline rather than being its cause. Thus, an evolutionary look into AD may shed new light on the currently still sombre perspectives regarding disease-modifying treatments of AD and prove useful as a root cause analysis.
{"title":"Evolutionary Considerations on Aging and Alzheimer's Disease","authors":"A. Gunten, Marie-Thérèse Clerc, R. Tomar, P. John-Smith","doi":"10.4172/2161-0460.1000423","DOIUrl":"https://doi.org/10.4172/2161-0460.1000423","url":null,"abstract":"Increasingly people are surviving into old age both in high and middle/low income countries. The increase in longevity is associated with increased levels of morbidity of both somatic and mental disorders during those added years. These pathologies prompt developing strategies for effective prediction, prevention and treatment of such disorders, among them the dementias such as Alzheimer’s disease (AD). Aging lies on a temporal continuum that starts at conception and ends at death. It refers to the aging processes occurring during an individual’s lifetime. However, our understanding of aging remains limited. In the early stages of dementia, distinguishing normal from pathological aging remains complex. Medical research customarily investigates the immediate mechanisms or pathogenesis of “how” diseases come about and affect patients. Evolutionary perspectives consider the reasons “why” people may have become particularly vulnerable to different conditions. Examining why people age is illuminating. Around the question whether aging is adaptive, we consider some evolutionary concepts useful around aging theories, among others antagonistic pleiotropy and life history theory and more recent concepts including evolvability and evolutionary developmental biology. As AD seems to be specific to homo sapiens, its existence may in part be anchored in the adaptive changes that have occurred after the hominidae separated from the pongidae. Around the question why apparently non-adaptive conditions such as AD are so frequent, we consider, among other aspects, brain development including the related phenomena of altriciality and grandmothering, the evolution of ApoE and the genome lag hypothesis. We consider the idea that the neuropathological hallmarks of AD help mitigate neurodegeneration and cognitive decline rather than being its cause. Thus, an evolutionary look into AD may shed new light on the currently still sombre perspectives regarding disease-modifying treatments of AD and prove useful as a root cause analysis.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"2793 1","pages":"1-12"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86494066","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 : 2018-01-01DOI: 10.4172/2161-0460.1000430
Yongxia Zhou
Commentary to Quantitative PET/MRI Evaluation and Application in Neurology Yongxia Zhou Department of Radiology, University of Pennsylvania, USA Introduction: With the high spatial resolution of magnetic resonance imaging (MRI) particularly for the soft tissue such as in brain and nonion radiation involved, the integrative positron emission tomography (PET)/ MRI system is expected to provide almost equivalent image quality compared with PET alone or PET/CT system, and simultaneous MRI information that is not conventionally available [1]. PET-MRI opens new horizons in multi-parametric neuroimaging for clinical research that allows simultaneous imaging of multiple parametric changes such as blood flow and metabolism at the same time. While MRI could provide superior structural information, applying MRI anatomical priors to reduce the PET partial volume effect could be achieved to improve spatial resolution of PET images for clinical and research usages. Objectives: Further applications in brain tumors and cancer response monitoring have reported complementary and valid information that this relatively new modality could achieve based on newly developed techniques. Newer and better MRIbased attenuation correction (AC) such as zero TE (ZTE) for more bone-related tissue signal detection and faster reconstruction compared to UTE/Dixon has been reported [36]. Advanced MRI-based motion correction for PET image reconstruction, newer PET time of flight reconstruction and incorporation with compressed sensing techniques have offered attractive superior temporal and spatial resolutions for disease diagnosis and prevention [7-9]. We briefly review the applications of PET/MRI in neurology with two examples in Alzheimer’s disease and brain tumor cases in this commentary.
PET/MRI定量评价及在神经病学中的应用述评由于磁共振成像(MRI)的高空间分辨率，特别是对脑部等软组织和涉及的非离子辐射，正电子发射断层扫描(PET)/ MRI一体化系统有望提供与单独PET或PET/CT系统几乎相同的图像质量，并同时提供传统上无法获得的MRI信息[1]。PET-MRI为临床研究开辟了多参数神经成像的新视野，允许同时成像多参数变化，如血流和代谢。虽然MRI可以提供更好的结构信息，但应用MRI解剖先验来降低PET部分体积效应可以提高PET图像的空间分辨率，用于临床和研究。目的:在脑肿瘤和癌症反应监测方面的进一步应用报告了补充和有效的信息，这种相对较新的模式可以基于新开发的技术实现。与UTE/Dixon相比，已经报道了更新、更好的基于mri的衰减校正(AC)，如zero TE (ZTE)，用于更多的骨相关组织信号检测和更快的重建[36]。先进的基于mri的PET图像重建运动校正，更新的PET飞行时间重建以及与压缩感知技术的结合为疾病诊断和预防提供了具有吸引力的优越时空分辨率[7-9]。本文以阿尔茨海默病和脑肿瘤为例，简要回顾PET/MRI在神经病学中的应用。
{"title":"Commentary to Quantitative PET/MRI Evaluation and Application in Neurology","authors":"Yongxia Zhou","doi":"10.4172/2161-0460.1000430","DOIUrl":"https://doi.org/10.4172/2161-0460.1000430","url":null,"abstract":"Commentary to Quantitative PET/MRI Evaluation and Application in Neurology Yongxia Zhou Department of Radiology, University of Pennsylvania, USA Introduction: With the high spatial resolution of magnetic resonance imaging (MRI) particularly for the soft tissue such as in brain and nonion radiation involved, the integrative positron emission tomography (PET)/ MRI system is expected to provide almost equivalent image quality compared with PET alone or PET/CT system, and simultaneous MRI information that is not conventionally available [1]. PET-MRI opens new horizons in multi-parametric neuroimaging for clinical research that allows simultaneous imaging of multiple parametric changes such as blood flow and metabolism at the same time. While MRI could provide superior structural information, applying MRI anatomical priors to reduce the PET partial volume effect could be achieved to improve spatial resolution of PET images for clinical and research usages. Objectives: Further applications in brain tumors and cancer response monitoring have reported complementary and valid information that this relatively new modality could achieve based on newly developed techniques. Newer and better MRIbased attenuation correction (AC) such as zero TE (ZTE) for more bone-related tissue signal detection and faster reconstruction compared to UTE/Dixon has been reported [36]. Advanced MRI-based motion correction for PET image reconstruction, newer PET time of flight reconstruction and incorporation with compressed sensing techniques have offered attractive superior temporal and spatial resolutions for disease diagnosis and prevention [7-9]. We briefly review the applications of PET/MRI in neurology with two examples in Alzheimer’s disease and brain tumor cases in this commentary.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"26 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74572921","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 : 2018-01-01DOI: 10.4172/2161-0460.1000411
Gokulraj T. Prabhakaran, Rajbir S. Bakshi
Objective: The purpose of this analysis is to understand the structure and change in costs for an established longitudinal study of Alzheimer’s disease with fixed enrollment. Methods: The examination begins with a discussion of the design of the consortium based study and the types of data collected by the researchers. Financial statements (2005 to 2017) are analyzed and forward projections are confirmed using linear regression. Funding is broken down by institution, with looks at per patient and personnel costs. Results: The rate of change for the costs is highly variable but correlated between institutions. Personnel costs are a critical driving factor. Per patient costs are noted to vary significantly between research institutions. The experiment will not be able to continue in its present form unless costs are brought to equilibrium with available funding. Sources of funding will need to consider opportunity costs, growth rates, and concurrent obligations as they evaluate projects. Conclusion: The longitudinal study is currently the most effective study design for progressive diseases. Funding for research does not align with the demonstrated need.
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Pub Date : 2018-01-01DOI: 10.4172/2161-0460.1000442
T. Ohm, V. Meske
The by far most relevant genetic risk factor for Alzheimer’s disease is possession of the allelic epsilon 4 variant of the cholesterol transporter apolipoprotein E. The apolipoprotein E allelic polymorphism impacts on both histopathological hallmarks of Alzheimer’s disease, the intraneuronal tau-aggregates forming neuropil threads and neurofibrillary tangles and the extracellular plaques built-up by beta-amyloid. Autophagy is a crucial process in neurons and plays a central role in cellular degradation of protein aggregates including those composed of tau or beta-amyloid. We discuss available evidence for a role of the apolipoprotein E polymorphism in autophagy.
{"title":"A New Role for ApoE-Not Only in Alzheimer's Disease?","authors":"T. Ohm, V. Meske","doi":"10.4172/2161-0460.1000442","DOIUrl":"https://doi.org/10.4172/2161-0460.1000442","url":null,"abstract":"The by far most relevant genetic risk factor for Alzheimer’s disease is possession of the allelic epsilon 4 variant of the cholesterol transporter apolipoprotein E. The apolipoprotein E allelic polymorphism impacts on both histopathological hallmarks of Alzheimer’s disease, the intraneuronal tau-aggregates forming neuropil threads and neurofibrillary tangles and the extracellular plaques built-up by beta-amyloid. Autophagy is a crucial process in neurons and plays a central role in cellular degradation of protein aggregates including those composed of tau or beta-amyloid. We discuss available evidence for a role of the apolipoprotein E polymorphism in autophagy.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"7 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74969887","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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