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Showing 3 results for Alzheimer Disease

Soheila Hosseinzadeh , Maryam Zahmatkesh , Gholam-Reza Hassanzadeh Hassanzadeh , Morteza Karimian , Mansour Heidari , Mahmoud Karami ,
Volume 73, Issue 8 (11-2015)
Abstract

Background: Seladin-1 protein protects the neural cells against amyloid beta toxicity and its expression decreased in vulnerable regions of Alzheimer's disease (AD) brains. On the other hand, changes in serum levels of S100 have been considered as a marker of brain damage in neurodegenerative diseases. Furthermore, this study was carried out to determine the relation between the change profile of serum S100&beta protein levels and hippocampal Seladin-1 gene expression in a rat model of sporadic AD. Methods: In this experimental study that established in Department of Neuroscience, School of Advanced Technologies in Medicine, Tehran University of Medical Science, from March 2011 to April 2013, 72 animals were randomly divided into control, 4, 7, 14, and 21days ICV-STZ/Saline administrated rats. Alzheimer's model was induced by intracerebroventricular (ICV) injections of streptozotocin (STZ) [3 mg/kg] on days 1 and 3. Serum levels of S100&beta and hippocampal Seladin-1 gene expression were evalu-ated in experimental groups. The initial and step-through latencies (STL) were deter-mined using passive avoidance test. Results: Serum levels of S100&beta were significantly different between the STZ-7 day and STZ-14 day groups in comparison with the control, saline and STZ-4 day groups. As well as, there was a significant difference between the STZ-7 day group in comparison with the STZ-14 day and STZ-21 day groups (P=0.0001). Hippocampal Seladin-1 gene expression in STZ-14 day and STZ-21 day groups significantly decreased as compared to the control, saline and STZ-4 day groups (P=0.0001). However, significant correla-tion was detected between serum S100&beta protein decrement and Seladin-1 down regula-tion (P=0.001). Also, the STL was significantly decreased in 21 days ICV-STZ adminis-trated rats as compared to the control or saline groups (P=0.001). Conclusion: Monitoring the changes of serum S100&beta protein levels by relationship with changes in hippocampal Seladin-1 gene expression can be a useful indicator of neu-ronal damage in patients with Alzheimer's disease.


Vajiheh Aghamollaii , Abbas Tafakhori , Shakila Meshkat , Arezoo Shafieyoun , Amir Salimi ,
Volume 78, Issue 1 (4-2020)
Abstract

Background: Alzheimer's disease (AD) is a chronic neurodegenerative disease characterized by a progressive decline of cognitive performance, which has a harmful impact on social activities. AD is the main cause of dementia and loss of functional independence in the elderly. AD is a worldwide concern because of its adverse consequences and expanding prevalence and incidence. Vitamin D is the most common nutritional deficiency worldwide among children and adults. In addition to its classical function of bone metabolism regulation, vitamin D exhibits multiple biological targets mediated by the vitamin D receptor (VDR). Vitamin D is a risk factor for a wide range of diseases and, as a neurosteroid, has an essential role in nervous system development and protection. Vitamin D regulates mechanisms involved in the pathogenesis of AD, including phagocytosis of amyloid-beta plaques, anti-inflammatory action, antioxidant action, regulation of intraneuronal calcium, ischemic zone size reduction, regulation of choline acetyltransferase enzyme and neurotrophic agents. This study aimed to evaluate the association between AD and vitamin D deficiency.
Methods: In this case-control study, 44 Alzheimer’s disease patients (diagnosed based on DSM-IV-TR criteria) compared with 40 patients that had no disease related to vitamin D. This study was performed in the neurology clinics of Roozbeh and Imam Khomeini Hospitals in Tehran, from April to March 2015. The demographic data were collected. After obtaining informed consent, venous blood was taken by clinical staff to measure the level of 25-hydroxyvitamin D3. Statistical analysis was performed on data.
Results: The Mean age was 71.55 years old (69.88 for females and 73.74 for males) in the case group. Mean vitamin D levels were 26.31 ng/ml and 36.41 ng/ml in case and control groups, respectively. Vitamin D level was deficient (< 30 ng/ml) in 75% of patients, of which 23% were severely deficient (< 10 ng/ml). Statistical analysis showed no significant relationship between Alzheimer's disease and vitamin D levels (P=0.057), but when participants categorized into three groups based on serum vitamin D levels (deficient, insufficient, sufficient), we found a significant relationship between them (P=0.019).
Conclusion: Our results confirm the association between vitamin D deficiency and Alzheimer's disease. Vitamin D supplementation should be considered in individuals at risk of Alzheimer's disease to reach sufficient vitamin D level.

Yunus Soleymani, Amir Reza Jahanshahi, Davood Khezerloo ,
Volume 80, Issue 11 (2-2023)
Abstract

Background: Atrophy of hippocampal subfields is one of the diagnostic biomarkers of Alzheimer's disease, which has also been observed in many patients with mild cognitive impairment. There is still no clear understanding of the atrophy pattern of hippocampal subfields in Alzheimer's disease and its differentiation from mild cognitive impairment. In this cross-sectional study, hippocampal subfield atrophy in Alzheimer's patients were compared with patients with early (EMCI) and late (LMCI) cognitive impairment and the control group.
Methods: This was a cross-sectional study conducted from September 2021 to September 2022 in the radiology department of Tabriz Paramedical Faculty. MRI images of Alzheimer's patients, EMCI patients, LMCI patients, and normal controls (NCs) were obtained from the ADNI database. Different hippocampus subfields of hippocampal fissure, dentate gyrus head, dentate gyrus body, first cornu ammonis body, cornu ammonis head, subiculum body, and subiculum head were isolated using the hippocampus segmentation tool in FreeSurfer 7.0 software. The volume of all subfields was calculated bilaterally and normalized. The volume difference of each hippocampus subfield between the groups participating in the study and the pair volume difference between the groups was analyzed using the Kruskal-Wallis H Test and post-hoc Dunn's test. The P<0.05 was considered as the significance level.
Results: The most significant volume difference between the four groups participating in the study was related to the whole hippocampus, DG body, subiculum body, and subiculum head subfields (P<0.0001). Also, when examining pairs, the most significant difference was observed between the NC/AD pair (P<0.0001) and the least significant difference between the pair of LMCI/AD group (P<0.05) and in the subfield subiculum body showing the progressive course of hippocampal subfield atrophy with cognitive progress towards Alzheimer's disease.
Conclusion: In most subfields of the hippocampus, a significant difference in atrophy can be seen, increasing the severity of atrophy as the disorder progresses toward Alzheimer's. Such findings can help guide future studies to improve diagnostic performance to identify individuals at high risk of Alzheimer's disease.


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