Journal of Alzheimers Disease & Parkinsonism最新文献

{"title":"Mild Cognitive Impairment: Implications of Diagnosis","authors":"Blake J. Lawrence, N. Gasson, A. Loftus","doi":"10.4172/2161-0460.1000422","DOIUrl":"https://doi.org/10.4172/2161-0460.1000422","url":null,"abstract":"","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"17 1","pages":"1-9"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80192566","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":"Applications of Repetitive Transcranial Magnetic Stimulation on Motor Symptoms in Parkinson's Disease","authors":"Y. Saitoh, T. Mano, M. Yokoe","doi":"10.4172/2161-0460.1000424","DOIUrl":"https://doi.org/10.4172/2161-0460.1000424","url":null,"abstract":"various cortical targets, including the primary motor cortex (M1), supplementary motor area (SMA), and left dorsolateral prefrontal cortex (DLPFC), has been reported. After application of high-frequency (HF)rTMS over the M1, most studies have demonstrated that PD patient’s exhibit improved motor function in their hands and gait [10-12]. The HF-rTMS over the M1 suggested being increased motor-related activity in the caudate nucleus. Even so, other studies have reported no beneficial effects of this stimulation [13]. In one study, an rTMS of 5 Hz over the SMA modestly improved motor symptoms in patients with PD [14]. Another study, which aimed to improve disturbance in mood in PD patients by applying rTMS over the DLPFC, demonstrated positive effects on depression level [15]. Moreover, a few other studies have reported positive effects and improvement in motor symptoms in PD patients who received rTMS over the DLPFC [16]. Therefore, optimal parameters for rTMS remain to be established. To address this issue, we sought to identify the best cortical area for HF-rTMS therapy in patients with PD by conducting a double-blind, placebo-controlled, crossover study. After application of HF-rTMS over the M1, SMA, DLPFC and sham, we compared the results to those obtained during sham stimulations [17]. This study reported that the UPDRS-III scores following the application of HF-rTMS over the M1 and SMA was significantly greater than that following sham stimulation. In contrast, changes in UPDRSIII scores following bilateral rTMS over the DLPFC were not different from those after sham stimulation. No significant changes emerged for either the depression or apathy scores following HF-rTMS over any cortical area. Therefore, application of HF-rTMS over the M1 and SMA significantly improved the motor symptoms in patients with PD but did not improve mood disturbances. Many positive studies report improvement of bradykinesia, but diverge in their efficacy to treat other cardinal symptoms of PD. rTMS improved gait in several [18,19], but not all studies [20]. A few studies have reported finding improvement in tremor symptoms in PD patients who received rTMS. At present, the mechanisms of rTMS in relation to disturbances in motor function and mood in PD remain unclear and thus controversial. A hypoactive caudate nucleus may underlie the motor deficits in PD patients by interfering with the normal functioning of the striato-frontal motor loop. Applying HF-rTMS over the M1 may partially compensate for the underactive basal ganglia-thalamocortical outflow to the frontal motor cortical areas","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"42 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":"72563324","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":"Does the Choice of Treatment of Diabetes Mellitus Change Natural Course of Alzheimer Disease","authors":"Emina Karahmet, B. Prnjavorac, Asja Sejranic, Esma Karahmet, A. Mujaković, K. Krajina, Amela Hasanović-Gogić, N. Delic","doi":"10.4172/2161-0460.1000415","DOIUrl":"https://doi.org/10.4172/2161-0460.1000415","url":null,"abstract":"Alzheimer disease (AD) is common worldwide and almost every case has comorbidities. One of the most common comorbidities of AD is Diabetes mellitus (DM), with or without metabolic syndrome. Both diseases effect nerve tissue and successful treatment would improve the status of the patient. In patients with Alzheimer disease treatment of DM, the treatment could be harmful to the AD, because of that high insulin intake. This may lead to progression of AD. Insulin is considered the best treatment for DM, but insulin therapy could increase comorbidity with AD. No specific therapy for AD is known up to date, so because of that DM is one of the most important risk for AD, concomitant therapy for DM should be planned very carefully. All options of DM therapy should be considered, and different mechanisms of anti-diabetic drugs are preferable. Treatment of AD is more complex metabolic syndrome is present. Any inflammation causes local tissue damage, including brain tissue during AD. Release of interleukins, primarily TNF-α, IL-6, IL-1β in the presence of adipokine leptin, maintains chronic inflammatory status in local brain tissue. Thus, low doses of immunosuppressant therapy should be considered for treatment of AD in future. To delay apoptosis of nerve tissue cells, brain and nerve tissue defend against free oxygen radicals and improve metabolic status.","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":"86008609","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":"Neuroinflammation in Preclinical Alzheimer's Disease: A Review of Current Evidence","authors":"T. Watermeyer, V. Raymont, K. Ritchie","doi":"10.4172/2161-0460.1000434","DOIUrl":"https://doi.org/10.4172/2161-0460.1000434","url":null,"abstract":"The pathology of sporadic Alzheimer’s disease (AD) may be present at mid-life and precede the prodromal and clinical dementia syndromes associated with the disorder by decades. Few successful therapeutic treatments exist and, as a result, attention is turning to the preclinical stages of the disease for the development of future intervention strategies. The success of such strategies will rely on well-defined biomarkers of preclinical disease to identify and monitor changes earlier in the disease course. Here, we consider whether immune function changes are potentially useful markers of preclinical disease. We have selected studies spanning epidemiological, animal, clinical and imaging research pertaining to the earliest stages of AD pathogenesis, as well as studies of non-demented adults at high AD risk. We examine changes in inflammatory markers, alongside changes in established biomarkers, to highlight their suitability as disease indicators across preclinical and prodromal stages. We conclude that further work surrounding this topic is required, calling for larger prospective epidemiological studies of preclinical disease that incorporate serial assessment designs with a wider range of inflammatory mediators. We anticipate that future benefits of work in this area include improved disease detection and modification, as well as diagnostic accuracy of trial participants, leading to more cost-effective observation and intervention studies.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"36 1","pages":"1-6"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78308146","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":"Age-Related Expression of Beta-Synuclein in the Ascending Visual Pathway and Comparative Analysis of its Function within the Neuroretina and Cerebral Cortex In-vitro","authors":"M. Böhm, Karina Hadrian, Katrin Brockhaus, Harutyn Melkonyan, S. Thanos","doi":"10.4172/2161-0460.1000427","DOIUrl":"https://doi.org/10.4172/2161-0460.1000427","url":null,"abstract":"Objective: Aging hampers visual function in a multifactorial manner and the underlying perceptual deficits cannot be explained by anatomical alterations of the eye and/or visual cortex alone. The aging process of structures of the Ascending Visual Pathway (AVP) between neuroretina and visual cortex is rarely studied. The age-related increase of Beta-Synuclein (SNCB) was detected in both the neuroretina and the visual cortex (V1) in different species. SNCB acts as a physiological antagonist to neurodegenerative disease -associated alpha-synuclein. The aim of the work was to explore expression patterns of SNCB within different parts of the AVP. Further, the role of SNCB in different targeted neuronal tissues was studied. Methods: The expressions of SNCB were compared in the newborn, juvenile, adult, and aged Optic Chiasm (OC), Tracuts Opticus (TO), Laterale Geniculate Nucleus (LGN), and superior colliculus (LGN) of rats. Western blot (WB), quantitative reverse-transcription polymerase chain reaction (qRT-PCR), and immunohistochemistry (IHC) analyses were employed to determine whether the changes identified by proteomics were verifiable at the cellular and molecular levels. To investigate the properties of SNCB in neuronal and glial cells, rat retinal and cortical samples (P5-7) were prepared and exposed to different SNCB concentrations up to 72 h in-vitro. The suspected influence on the expression on neuronal cells (e.g., beta III tubulin) and glial cell (e.g., glial fibrillary acidic protein) as well as apoptosis markers (e.g., TUNEL) was assessed by IHC, WB, and qRT-PCR. In addition, the p53-MDM2 signalling pathway was studied by IHC. Results: An increase of SNCB expression was detected in all examined regions of the AVP. Main differences of SNCB expression regarding to associated cell types were found in OC and TO in comparison to LGN and SC. The detected protein alterations in OC and TO were analogous to recent reports of the retinal profiles, while the SNCB expression characteristics in LGN and SC were more comparable to the characteristics within cortical tissues. Differences in response to SCNB exposure were found between retinal and cortical cells in-vitro. A loss of neuronal cells together with an increased apoptosis has been found in retinal cultures. In contrast, cortical cells show a beneficial elevation of neuronal response after SNCB exposure. While SNCB-exposed neuroretina show an activation of the p53-MDM-2 signaling, a decreased activation of p53-MDM-2 singanling pathway in cortical cells has been found. Conclusions: This study is the first to provide evidence that SNCB expression is associated with postnatal maturation and aging in the AVP of rats. Moreover, SNCB may exert different effects on several cell subtypes within selected neuronal targets like neuroretina and cortex. The findings may indicate the role of SNCB in key functional pathways and may account for the onset and/or progression of age-related pathologies. Further st","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"31 1","pages":"1-14"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88824189","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":"Immunoreactivity of Anti-AβP-42 Specific Antibody with Toxic Chemicals and Food Antigens","authors":"A. Vojdani, E. Vojdani","doi":"10.4172/2161-0460.1000441","DOIUrl":"https://doi.org/10.4172/2161-0460.1000441","url":null,"abstract":"Objective: The aim of our study was to examine immunoreactivity between AβP-42, toxic chemicals, and food proteins that could be involved in AD. Methods: We applied monoclonal anti-AβP-42 to a variety of chemicals bound to human serum albumin (HSA) and 208 different food extracts. Results: We found that anti-AβP-42 reacts from moderately to strongly with mercury-HSA, dinitrophenyl-HSA (DNP-HSA), phthalate-HSA, and aluminum-HSA, but not to many other tested chemicals bound to HSA nor to HSA alone. This antibody also reacted with 19 out of the 208 food antigens used in the assay. One example of a food that reacted strongly with anti-AβP-42 in our study was canned tuna, although raw tuna reacted only moderately. Conclusion: Based on these results, we hypothesized that reaction between AβP-42 antibody with chemicals bound to HSA and numerous food antigens might play a role in Alzheimer’s disease (AD). These anti-AβP antibodies could be derived from protein misfolding similar to β-amyloid, or from antibodies to various food antigens that cross-react with AβP-42. Removal of toxic chemicals and food items that share a homology with β-amyloid may be recommended at least for patients in the early stages of AD. Therefore, the role of AβP-42 cross-reactive foods and chemicals bound to HSA in neurodegeneration should be investigated further.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"173 1","pages":"1-11"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90049590","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":"Vegetable Oil: The Real Culprit behind Alzheimer’s Disease","authors":"T. Yamashima","doi":"10.4172/2161-0460.1000410","DOIUrl":"https://doi.org/10.4172/2161-0460.1000410","url":null,"abstract":"Its major component, polyunsaturated fatty acids (PUFA), is transported to all body organs via the blood, where it becomes a major component of cell membrane. Most “vegetable oil” consists of ω-6 PUFA of which linoleic acid is the major constituent, such as soybean oil, corn oil, rapeseed oil, and safflower oil. If deep-fried dishes are cooked by heating “vegetable oil” that contains large amounts of linoleic acid to 150-200°C, after 5 min, cytotoxic hydroxynonenal starts to form in the oil and reaches a high concentration in the food only 30 min later.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"68 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2017-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89367248","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":"Lithium in the Normal Therapeutic Range: A Potential Sneaky Danger for the Brain. A Case of Slow Tricking Neurotoxicity and a Brief Overview of Literature","authors":"E. Farina, L. Giani, C. Lovati, C. Mariani, R. Nemni","doi":"10.4172/2161-0460.1000407","DOIUrl":"https://doi.org/10.4172/2161-0460.1000407","url":null,"abstract":"In medicine, Lithium salts are known to be useful as a mood-stabilizing drug in the treatment of bipolar disorder and depression. In neurology Lithium is used as prophylaxis of cluster headache. Lithium may induce intoxication with renal failure, thyroid dysfunction, cardiac arrhythmias and neurotoxicity. Toxicity signs are associated with increased serum concentrations (>1.2 mEq/l); however, there have been some reports of neurotoxicity also with therapeutic drug levels. We describe the case of a 70 years old woman who was assuming Lithium for a bipolar disorder with a permanent control of psychiatric symptoms. After 40 years of continued therapy with lithium she developed a rapidly progressive dementia with multifocal brain signs, although lithium serum levels were always normal. She was carefully investigated with regard to the cognitive decline and all possible primary and secondary rapidly progressive dementia were excluded. When the clinical state was quite terminal, all therapies were interrupted and she progressively recovered after withdrawal of lithium therapy.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"84 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2017-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90722995","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":"Recurrent Head Trauma: A Trigger of the Alzheimer Cascade or the Cause of an Independent Pathologic Entity? - An Explicative Case of Chronic Traumatic Encephalopathy Mimicking Alzheimer's Disease","authors":"G. Grande, D. Galimberti, L. Maggiore, E. Scarpini, C. Mariani, C. Lovati","doi":"10.4172/2161-0460.1000408","DOIUrl":"https://doi.org/10.4172/2161-0460.1000408","url":null,"abstract":"Repeated traumatic brain injuries have a negative impact on brain integrity and cognition. It was hypothesized that they could trigger the AD amyloidogenic cascade or they could represent a peculiar clinical entity labelled as “chronic traumatic encephalopathy”, CTE. To contribute in the understanding of this controversy we describe the case of a boxer with early onset dementia, reporting biomarkers and neuropsychological assessment with the effort to differentiate the AD diagnosis and CTE. We discuss, for each element, it’s possible role with regard to the opposite diagnostic directions and we highlight, on the example of our probable CTE patient, the necessity of better defined diagnostic criteria for the chronic traumatic encephalopathy.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"56 1","pages":"1-4"},"PeriodicalIF":0.0,"publicationDate":"2017-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91386077","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":"Evidence-Based Review of Therapeutic Approaches in Dementia with Lewy Bodies","authors":"A. Ouf, K. Szigeti","doi":"10.4172/2161-0460.1000406","DOIUrl":"https://doi.org/10.4172/2161-0460.1000406","url":null,"abstract":"Dementia with Lewy Bodies (DLB) is estimated to affect around 15-20% of dementia cases globally. This places it as the second most common type of dementia after Alzheimer’s disease (AD). Paradoxically, clinical trials addressing the complex symptomatology of DLB are sparse compared to AD. While substantial progress has been made in overcoming the diagnostic challenges, evidence-based treatment is elusive. In this review we summarize the available placebo-controlled clinical trials and identify areas of need to develop treatment strategies.","PeriodicalId":15012,"journal":{"name":"Journal of Alzheimers Disease & Parkinsonism","volume":"1961 1","pages":"1-5"},"PeriodicalIF":0.0,"publicationDate":"2017-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91244266","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}