Journal of Alzheimers Disease & Parkinsonism最新文献

{"title":"Age-Dependent Cognitive Sequelae of Advanced Carotid Disease after CarotidEndarterectomy","authors":"I. Popović, I. Lovričević, A. Popović, A. Lovrenčić‐Huzjan","doi":"10.4172/2161-0460.1000527","DOIUrl":"https://doi.org/10.4172/2161-0460.1000527","url":null,"abstract":"","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"32 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2021-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89579718","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}

{"title":"To Investigate Role of Glycosylated Hemoglobin (Hba1c) as a Biomarker for Prediction of Dementia and Cognitive Dysfunction in Type 2 Diabetic Patients","authors":"Aman Gupta, A. Singh, R. Deka, Rakesh K. Gupta, Ritu Jha","doi":"10.4172/2161-0460.1000437","DOIUrl":"https://doi.org/10.4172/2161-0460.1000437","url":null,"abstract":"Introduction: Diabetes Mellitus is one the major disease burden globally. One of the significant complications of the uncontrolled Diabetics is Cognitive dysfunction and Dementia. In this study we laid focus on the Evaluation of HbA1C as a Biomarker to predict Dementia and Cognitive Dysfunction in Type 2 Diabetic Mellitus. Aim of the study: A pilot study to investigate HbA1C as a Biomarker for prediction of Dementia and Cognitive Dysfunction in Type 2 Diabetic Mellitus in a Hospital Setting. Methods and results: A prevalence study in which 60 subjects (n=30 Type 2 Diabetics; n=30 non Diabetic) were enrolled. In this study HbA1C values were correlated with that of individual memory and cognition batteries* score. The range of the HbA1C values was 7.1 to 13.3. The mean values of HbA1C in the Diabetic group (n=30) was found to be 9.19.The corresponding values of Pearson’s Correlation “r” in the diabetic group of the w.r.t. various Cognitive batteries were: General Practitioner Assessment of Cognition (GPCOG)=-0.53; Attendant Informant Tool (AI)=-0.43; Memory Impairment Screen (MIS)=-0.37; Negative values of the Pearson’s Correlation “r” indicates that lower the respective battery score, poorer is the cognitive function. In the Diabetic group GPCOG, AI and MIS were found to be significantly correlated with HBA1C. Similarly, in the non- Diabetic group (n=30), no significant Dementia and Cognitive Impairment was recorded when same group of Cognitive Batteries were administered. Conclusion: It is quite evident from the results that HbA1C as biomarker has a great potential to predict Dementia and Cognitive decline in uncontrolled Diabetes. However, the study needs to be conducted on a larger scale along with comparative analysis with tools like Functional MRI and other standard biomarkers.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"33 1","pages":"1-8"},"PeriodicalIF":0.0,"publicationDate":"2018-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88319326","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}

{"title":"Disrupted Blood-CSF Barrier to Urea and Creatinine in Mild Cognitive Impairment and Alzheimer's Disease","authors":"Conrad E. Johansona, E. Stopa, L. Daiello, S. Monte, Matthew Keane, B. Ott","doi":"10.4172/2161-0460.1000435","DOIUrl":"https://doi.org/10.4172/2161-0460.1000435","url":null,"abstract":"Objective: In this pilot study hypothesizing that blood-CSF barrier (BCSFB) function is altered in mild cognitive impairment (MCI), we evaluated small-sized biomarker distribution between serum (SER) and cerebrospinal fluid (CSF). For both MCI and Alzheimer (AD) patients we quantified CSF neurochemistry; and compared CSF/SER ratios for urea and creatinine, as well as albumin, to those of healthy controls. Methods: A compromised BCSFB in neurodegenerative states alters CSF-to-serum (CSF/SER) concentrations. We analyzed urea, creatinine and albumin, for transbarrier (across choroid plexus) distribution between CSF and serum, from patients with MCI (n=8) or AD (n=13). Lumbar CSF and arterial blood were frozen/analyzed by multiplex technology. Results: In healthy controls, the CSF creatinine was significantly concentrated ~50% above the serum level. In both MCI and AD, the CSF creatinine concentration decreased while the urea level increased; CSF albumin was also elevated in AD. CSF/SER ratios for controls, MCI and AD were: urea 0.80, 0.98, 0.86; creatinine 1.52, 1.13, 1.14; and albumin 0.0045, 0.0051, 0.0065. Thus, CSF/SER ratios for creatinine and urea in MCI were similar to those in AD patients. Conclusion: Blood-CSF barrier compromise in MCI resembled that in AD. In cognitively-impaired patients, the dissipating ratios toward equilibrium suggest disease-altered BCSFB permeability (urea and albumin) and transporter activity (creatinine/creatine). We propose that redistribution of urea and creatinine, between serum and CSF, are useful biomarkers for evaluating disease-induced alterations in CSF biochemistry and BCSFB functional status.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"15 2","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2018-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91442016","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}

{"title":"Correlation of Alzheimer’s Dementia Markers","authors":"H. Akhondi","doi":"10.4172/2161-0460.1000432","DOIUrl":"https://doi.org/10.4172/2161-0460.1000432","url":null,"abstract":"Introduction: Alzheimer’s disease remains a major cause of morbidity, mortality and dependency in older patients with dementia. With increasing age in older population and dementia in western hemisphere, an inexpensive and unified modality for early diagnosis of AD is of utmost importance. Methods: We sought to investigate single photon emission computed tomography (SPECT) imaging of the brain as a less expensive modality in a prospective single blinded study in a cohort with diagnosis of probable Alzheimer’s dementia. Patients’ demographics, family history, Mini Mental Status Exam, brain imaging, biomarkers such as Tau, Amyloid beta protein, and Apo E genotype were obtained and analyzed. We tested different possible correlations models for association of current diagnosis of Alzheimer’s disease with SPECT and biomarkers using Chi-square test. Results: Biochemical markers (Amyloid beta 42 and tau protein) have higher sensitivity in identifying patients with AD. APOE genotype is less sensitive as a diagnostic test. SPECT did not correlate with biomarkers in early AD, but showed higher correlation in moderate and severe dementia. Further investigation is warranted to identify a more sensitive and specific yet inexpensive testing for early diagnosis of AD. Discussion: Biochemical and genetic markers have a closer association with each other and with Alzheimer’s compared to their association with brain imaging of patients with Alzheimer’s disease.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"1 1","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"2018-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76140012","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}

{"title":"Apathy in Huntington’s Disease: A Review of the Current Conceptualization","authors":"M. Camacho, R. Barker, S. Mason","doi":"10.4172/2161-0460.1000431","DOIUrl":"https://doi.org/10.4172/2161-0460.1000431","url":null,"abstract":"Apathy is one of the most common psychiatric symptoms experienced by patients with Huntington’s disease (HD). It appears early, progresses with the disease course and has been shown to contribute significantly to caregiver burden. However, what is understood by apathy in HD is not clearly defined nor the underlying mechanisms responsible for it. In this review, we discuss the concept of apathy in the context of HD and propose that a consensus regarding its conceptualisation and subsequently its diagnostic criteria would significantly benefit the field. In order to undertake this work, we began by reviewing the existing literature on the definition and assessment of apathy in HD, its underlying neurobiological basis and its relationship to other related features such as abulia, anhedonia and alexithymia. In the context of HD, apathy could be described by a loss of or diminished motivation, emotion and goal-directed behaviour that is not best explained by motor or social constraints of the disease. However, there is an urgent need to better understand the characteristics of apathy specifically in HD, how they evolve across the disease course and how they relate to central dopaminergic pathways. Only by undertaking such work can we hope to better understand this early and disabling aspect of HD.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"3 1","pages":"1-9"},"PeriodicalIF":0.0,"publicationDate":"2018-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86770121","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}

{"title":"A Novel Dementia Scale for Alzheimer's Disease","authors":"Takashi Kikuchi, Takahiro Mori, K. Wada-isoe, Y. Umeda-Kameyama, T. Kagimura, S. Kojima, M. Akishita, Yu Nakamura","doi":"10.4172/2161-0460.1000429","DOIUrl":"https://doi.org/10.4172/2161-0460.1000429","url":null,"abstract":"Objective: We established the diagnostic accuracy of the “ABC Dementia Scale” (ABC-DS) for Alzheimer’s disease (AD), which concurrently assesses activities of daily living (“A”), behavioral and psychological symptoms of dementia (“B”), and cognitive function (“C”), using a novel scoring approach called the three-dimensional distance (TDD). \u0000Methods: The ABC-DS has 13 items with nine ordered categorical levels. Caregivers were interviewed using a semi-structured interview. The construct validity, concurrent validity, test-retest reliability, and responsiveness (score changes over 12 weeks) were assessed. \u0000Results: We enrolled 63 participants with probable AD as well as 88, 106, and 55 patients with mild, moderate, and severe AD, respectively. The construct and concurrent validities of each domain score were determined. The TDD accurately discriminated the AD stages and detected score changes indicating disease progression over 12 weeks. \u0000Conclusion: The ABC-DS is stable, accurately stages AD severity, and monitors disease progression. The TDD is a useful algorithm for detecting disease progression.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"1 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2018-03-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87448962","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}

{"title":"Is Preservation of Cholinergic Activation a Mechanism Underlying Cognitive Reserve","authors":"N. Matsukawa","doi":"10.4172/2161-0460.1000425","DOIUrl":"https://doi.org/10.4172/2161-0460.1000425","url":null,"abstract":"The cognitive reserve, despite having abundant pathological change of Alzheimer’s disease, some patients can preserve cognitive function, is a new concept to puzzle Alzheimer’s pathogenesis. Interestingly, some recent epidemiological study has shown that diet, exercise, cognitive training and vascular risk monitoring interventions may reduce cognitive decline in at-risk elderly people in the general population. However, the mechanisms underlying this cognitive function preservation are still unknown. Our recent data suggest that differences in the persisting degree of cholinergic activity might be, at least in part, involved in the decorrelation between the extent of cognitive deterioration and AD pathological changes. This fact might raise a possibility of cholinergic modulation for hippocampal glutamatergic activity in a mechanism of “cognitive reserve”.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"300 1","pages":"1-2"},"PeriodicalIF":0.0,"publicationDate":"2018-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76479537","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}

{"title":"The Correlation between Genotype and Phenotype of Alzheimer's Disease","authors":"H. L. Li, Bin Jiang, Zhi-Ying Wu","doi":"10.4172/2161-0460.1000417","DOIUrl":"https://doi.org/10.4172/2161-0460.1000417","url":null,"abstract":"Alzheimer’s disease (AD) is the most frequent cause of dementia, it manifests as a progressive decline in memory and other cognitive domains. The genetics of AD is complex and heterogeneous. Most cases are “sporadic late onset”, however, a small percentage of cases have an early onset and usually aggregate within families. Early studies revealed that a number of genes, including both rare mutations and common polymorphisms, play an important role in the development of AD. More recently it has been proposed that genetic variation may also explain some of the other features of clinical phenotype, such as age at onset, disease duration, cognitive decline, behavioral and psychiatric symptoms and so on. In this review, we compared the clinical phenotypes of reported mutations within the three causative genes and some common polymorphisms, with an emphasis on their heterogeneity. Hopefully, the unique phenotypic features of individual mutation will enable us to study molecular mechanisms, potentially explaining phenotypic differences and providing useful knowledge for the development of new therapeutic agents.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"41 1","pages":"1-9"},"PeriodicalIF":0.0,"publicationDate":"2018-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88016589","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}

{"title":"Lifetime Expectancy in Dementia with Lewy Bodies: Effects of Donepezil Administration and Special Nursing Home Replacement. A Retrospective Analysis in the Tajiri Project","authors":"K. Meguro, Keiichi Kumai, J. Takada, Keiko Chida, Yuriko Kato, S. Yamaguchi","doi":"10.4172/2161-0460.1000416","DOIUrl":"https://doi.org/10.4172/2161-0460.1000416","url":null,"abstract":"Objective: Cholinesterase inhibitors (ChEIs) can delay the progression of Alzheimer disease (AD). We previously demonstrated a positive effect of donepezil (DNP) administration and a Special Nursing Home (SNH) replacement on lifetime expectancy after the onset of AD. Recently DNP has been indicated for use in the treatment of dementia with Lewy Bodies (DLB); however, the effect on lifetime expectancy remains unclear. Herein, we analyzed the effects of DNP on DLB. \u0000Methods: All outpatients at the Tajiri Clinic with available medical records and death certificates from 1999- 2012 were included in this retrospective analysis. The entry criteria were a diagnosis of dementia based on DSM-IV criteria and diagnosis of DLB using the international consensus criteria; medical treatment for more than 3 months and follow up to less than 1 year before death. \u0000Results: We identified 510 subjects based upon medical records and death certificates, of which 360 had a diagnosis of dementia that met the entry criteria. Of 51 patients diagnosed with DLB, 23 had taken DNP and 28 patients had not undergone drug treatment due to treatment prior to the introduction of DNP in 1999 in Japan. The lifetime expectancies after onset were 6.4 years in the DNP group and 3.6 years in the non-DNP group; with a significant drug effect. However, in contrast with the previous AD data, no significant effect of SNH residency was noted. \u0000Conclusion: Although this report has the limitation that all analyses were retrospective and lacked randomization, we found a positive effect of DNP on lifetime expectancy after the onset of DLB. The lower life expectancy compared with that of AD and the lack of an effect of SNH residency suggest the cholinergic deficiency in DLB is greater than that in AD.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"30 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2018-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83182183","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}

{"title":"Mitochondrial Complex I Deficit in the Olfactory Systems of Age-related Neurodegenerative Monkey Models: A PET Study using 18F-BCPP-EF","authors":"F. Hashimoto, H. Ohba, Masakatsu Kanazawa, S. Nishiyama, T. Kakiuchi, H. Tsukada","doi":"10.4172/2161-0460.1000433","DOIUrl":"https://doi.org/10.4172/2161-0460.1000433","url":null,"abstract":"Objective: Dysfunction of olfactory bulb area (OBA) is reported in several types of neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. Although pathophysiological mechanisms responsible for changes in olfactory function remain unclear, the quantitative parameters for olfactory function are expected for diagnose of neurodegenerative diseases. We developed a novel probe for positron emission tomography (PET), 18F-2-tert-butyl-4-chloro-5-{6-[2-(2-fluoroethoxy)-ethoxy]-pyridin-3-ylmethoxy}-2H-pyridazin-3-one (18F-BCPP-EF), for quantitative analysis of mitochondrial complex I (MC-I) activity in the living brain. In the present study, the applicability of 18F-BCPP-EF to predict age-related neurodegenerative damage in the monkey brain as an MC-I deficit in the OBA was investigated. Methods: PET measurements with 11C-PiB for amyloid--β (Aβ), 11C-DPA-713 for translocator protein (TSPO) and 18F-BCPP-EF were performed in aged monkeys. The binding specificity of 18F-BCPP-EF to MC-I in the OBA was evaluated with rotenone, a specific MC-1 inhibitor, in young animals. 11C-PiB binding to Aβ and 11C-DPA-713 binding to TSPO were calculated as standard uptake value ratios (SUVRs). The total distribution volume (VT) of 18F-BCPP-EF was calculated using a Logan graphical analysis using metabolite-corrected plasma input function, and correlations between the olfactory VT of 18F-BCPP-EF and SUVRs of 11C-PiB or 11C-DPA-713 in several brain regions were analyzed. Results: Pre-dosing of rotenone resulted in the significant reduction of VT values in all brain regions including the OBA. MC-I activity in the OBA exhibited age-related reduction, which positively correlated with MC-I activity in the olfactory-related and cortical regions. OBA MC-I and TSPO as measured using 11C-DPA-713 were inversely correlated in the olfactory-related and cortical regions, but association between OBA MC-I and Aβ deposition as measured using 11C-PiB were observed only in olfactory-related regions. Conclusion: The present study demonstrated that OBA MC-I activity could be a potential predictive parameter of neurodegenerative damages related Aβ deposition and TSPO/neuroinflammation in the living brain.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"26 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76362140","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}