scholarly journals A survey of community awareness of Alzheimer's disease: what are the common misconceptions?

2008 ◽  
Vol 23 (12) ◽  
pp. 1320-1322 ◽  
Author(s):  
Karen Sullivan
Author(s):  
Mohammad Azizur Rahman ◽  
Kamrul Islam ◽  
Saidur Rahman ◽  
Md Alamin

Abstract COVID-19, the global threat to humanity, shares etiological cofactors with multiple diseases including Alzheimer’s disease (AD). Understanding the common links between COVID-19 and AD would harness strategizing therapeutic approaches against both. Considering the urgency of formulating COVID-19 medication, its AD association and manifestations have been reviewed here, putting emphasis on memory and learning disruption. COVID-19 and AD share common links with respect to angiotensin-converting enzyme 2 (ACE2) receptors and pro-inflammatory markers such as interleukin-1 (IL-1), IL-6, cytoskeleton-associated protein 4 (CKAP4), galectin-9 (GAL-9 or Gal-9), and APOE4 allele. Common etiological factors and common manifestations described in this review would aid in developing therapeutic strategies for both COVID-19 and AD and thus impact on eradicating the ongoing global threat. Thus, people suffering from COVID-19 or who have come round of it as well as people at risk of developing AD or already suffering from AD, would be benefitted.


2021 ◽  
Author(s):  
Piyali Majumder ◽  
Kaushik Chanda ◽  
Debajyoti Das ◽  
Brijesh Kumar Singh ◽  
Partha Chakrabarti ◽  
...  

Alzheimer’s Disease (AD) and Type 2 Diabetes (T2D) share a common hallmark of insulin resistance. Reportedly, two non-canonical Receptor Tyrosine Kinases (RTKs), ALK and RYK, both targets of the same micro RNA miR-1271, exhibit significant and consistent functional downregulation in post-mortem AD and T2D tissues. Incidentally, both have Grb2 as a common downstream adapter and NOX4 as a common ROS producing factor. Here we show that Grb2 and NOX4 play critical roles in reducing the severity of both the diseases. The study demonstrates that the abundance of Grb2 in degenerative conditions, in conjunction with NOX4, reverse cytoskeletal degradation by counterbalancing the network of small GTPases. PAX4, a transcription factor for both Grb2 and NOX4, emerges as the key link between the common pathways of AD and T2D. Downregulation of both ALK and RYK through miR-1271, elevates the PAX4 level by reducing its suppressor ARX via Wnt/b-Catenin signaling. For the first time, this study brings together RTKs beyond Insulin Receptor (IR) family, transcription factor PAX4 and both AD and T2D pathologies on a common regulatory platform.


2020 ◽  
Vol 7 (1) ◽  
pp. 1-11
Author(s):  
Tammanna R. Sahrawat ◽  
Jyoti Dwivedi

Ageing is associated with a number of diseases. Alzheimer’s disease (AD) and diabetes are among such most common diseases. These two diseases are considered to be fundamentally similar disorders because they share some common elements, though they differ in the time of onset, tissues affected as well as the magnitudes of their specific traits. The present study was undertaken to prospect the association between the genes involved in Diabetes and AD; and their common pathophysiology. Using a network system biology approach, the genes common between Diabetes and AD were retrieved from DisGeNET database. The common genes were analysed using in silico tool, Cyctoscape’s various plug-ins, ClusterONE, CytoHubba, ClueGO and CluePedia. Eleven genes which can act as potential marker for both Diabetes and AD namely IL4, ICAM1, ALB, INS, CSF2, IL6, TNF, IL10, GAPDH, TLR4, and AKT have been identified in the present study. This is the first study of its kind in which relationship between Diabetes and AD has been investigated to identify their common genes, which can help in better understanding of pathophysiology of these age-related diseases.


2021 ◽  
Vol 6 (3) ◽  
pp. 322-326
Author(s):  
Dipak Kumar Dhar

Dementia broadly refers to a global decline in cognitive and higher functions of the brain. With the gradually increasing number of aging population, the incidence of dementia has been steadily rising and expected to increase further in the coming years. The causes and forms of dementia are wide-ranging and diverse, with Alzheimer’s disease being its best studied form. With increasing knowledge about various effects and mechanisms of nitric oxide, this chemical neurotransmitter appears to be the connecting link in the cellular pathogenesis of dementia. An exhaustive search of research articles, commentaries and books published from 1990s onwards was performed with various words and combinations linked to dementia and nitric oxide. The existing medical literature shows both neuroprotective and neurotoxic effects of nitric oxide. The present article intends to delve into this topic and provide a lucid understanding of the role of nitric oxide in dementia. Keywords: Dementia, Nitric Oxide, Alzheimer’s disease, excitotoxicity, nitrosative stress.


2021 ◽  
pp. 1-8
Author(s):  
Liling Dong ◽  
Chenhui Mao ◽  
Caiyan Liu ◽  
Jie Li ◽  
Xinying Huang ◽  
...  

Background: The previous studies have identified several genes in relation to Alzheimer’s disease (AD), such as ABCA7, CR1, etc. A few studies have explored the association between the common variants, mainly in the non-coding regions of these genes, and cerebrospinal fluid (CSF) biomarkers. Fewer studies target the variants in the coding regions. Objective: To illustrate the association between the common variants within or adjacent to the coding regions of AD susceptible genes and CSF biomarkers in AD patients. Methods: 75 sporadic probable AD patients were extracted from the dementia cohort of Peking Union Medical College Hospital. They all had history inquiry, physical examination, blood test, cognitive assessment, brain MRI, CSF testing of Aβ42, 181p-tau, and t-tau, and next-generation DNA sequencing. Sixty-nine common single nucleotide polymorphisms (SNPs) (minor allele frequency > 0.01) within or near the coding region of 13 AD susceptible genes were included in the analysis. Results: The rs7412-CC (APOE) genotype showed lower CSF Aβ42 level and higher p-tau/Aβ42 ratio than the rs7412-CT genotype. The rs3752246-C (ABCA7) allele correlated with lower CSF Aβ42 level. The alternate alleles of six ABCA7 SNPs were related to lower CSF p-tau, including rs3745842, rs3764648, rs3764652, rs4147930, rs4147934 and rs881768. The rs11609582-TT (A2M) genotype showed higher CSF p-tau than the rs11609582-TA genotype. The p-tau/Aβ42 ratio was higher in the rs490460-TT (BACE1) genotype relative to the rs490460-GT genotype. Conclusion: Some common variants within or near the coding regions of APOE, ABCA7, A2M, and BACE1 are associated with CSF Aβ42, p-tau. or p-tau/Aβ42.


2020 ◽  
Vol 28 (1) ◽  
pp. 19-52 ◽  
Author(s):  
Renu Chandra Segaran ◽  
Li Yun Chan ◽  
Hong Wang ◽  
Gautam Sethi ◽  
Feng Ru Tang

Radiation exposure may induce Alzheimer's disease (AD), depression or schizophrenia. A number of experimental and clinical studies suggest the involvement of miRNA in the development of these diseases, and also in the neuropathological changes after brain radiation exposure. The current literature review indicated the involvement of 65 miRNAs in neuronal development in the brain. In the brain tissue, blood, or cerebral spinal fluid (CSF), 11, 55, or 28 miRNAs are involved in the development of AD respectively, 89, 50, 19 miRNAs in depression, and 102, 35, 8 miRNAs in schizophrenia. We compared miRNAs regulating neuronal development to those involved in the genesis of AD, depression and schizophrenia and also those driving radiation-induced brain neuropathological changes by reviewing the available data. We found that 3, 11, or 8 neuronal developmentrelated miRNAs from the brain tissue, 13, 16 or 14 miRNAs from the blood of patient with AD, depression and schizophrenia respectively were also involved in radiation-induced brain pathological changes, suggesting a possibly specific involvement of these miRNAs in radiation-induced development of AD, depression and schizophrenia respectively. On the other hand, we noted that radiationinduced changes of two miRNAs, i.e., miR-132, miR-29 in the brain tissue, three miRNAs, i.e., miR- 29c-5p, miR-106b-5p, miR-34a-5p in the blood were also involved in the development of AD, depression and schizophrenia, thereby suggesting that these miRNAs may be involved in the common brain neuropathological changes, such as impairment of neurogenesis and reduced learning memory ability observed in these three diseases and also after radiation exposure.


2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Simone Eggert ◽  
Stefan Kins ◽  
Kristina Endres ◽  
Tanja Brigadski

Abstract Brain-derived neurotrophic factor (BDNF) is an important modulator for a variety of functions in the central nervous system (CNS). A wealth of evidence, such as reduced mRNA and protein level in the brain, cerebrospinal fluid (CSF), and blood samples of Alzheimer’s disease (AD) patients implicates a crucial role of BDNF in the progression of this disease. Especially, processing and subcellular localization of BDNF and its receptors TrkB and p75 are critical determinants for survival and death in neuronal cells. Similarly, the amyloid precursor protein (APP), a key player in Alzheimer’s disease, and its cleavage fragments sAPPα and Aβ are known for their respective roles in neuroprotection and neuronal death. Common features of APP- and BDNF-signaling indicate a causal relationship in their mode of action. However, the interconnections of APP- and BDNF-signaling are not well understood. Therefore, we here discuss dimerization properties, localization, processing by α- and γ-secretase, relevance of the common interaction partners TrkB, p75, sorLA, and sortilin as well as shared signaling pathways of BDNF and sAPPα.


2021 ◽  
pp. 1-12
Author(s):  
Jianlin Wang ◽  
Pan Wang ◽  
Yuan Jiang ◽  
Zedong Wang ◽  
Hong Zhang ◽  
...  

Background: The hippocampus with varying degrees of atrophy was a crucial neuroimaging feature resulting in the declining memory and cognitive function in Alzheimer’s disease (AD). However, the abnormal dynamic functional connectivity (DFC) in both white matter (WM) and gray matter (GM) from the left and right hippocampus remains unclear. Objective: To explore the abnormal DFC within WM and GM from the left and right hippocampus across the different stages of AD. Methods: Current study employed the OASIS-3 dataset including 43 mild cognitive impairment (MCI), 71 pre-mild cognitive impairment (pre-MCI), and matched 87 normal cognitive (NC). Adopting the FMRIB’s Integrated Registration and Segmentation Tool, we obtained the left and right hippocampus mask. Based on above hippocampus mask as seed point, we calculated the DFC between left/right hippocampus and all voxel time series within whole brain. One-way ANOVA analysis was performed to estimate the abnormal DFC among MCI, pre-MCI, and NC groups. Results: We found that MCI and pre-MCI groups showed the common abnormalities of DFC in the Temporal_Mid_L, Cingulum_Mid_L, and Thalamus_L. Specific abnormalities were found in the Cerebelum_9_L and Precuneus of MCI group and Vermis_8 and Caudate_L of pre-MCI group. In addition, we found that DFC within WM regions also showed the common low DFC for the Cerebellum anterior lobe-WM, Corpus callosum, and Frontal lobe-WM in MCI and pre-MCI group. Conclusion: Our findings provided a novel information for discover the pathophysiological mechanisms of AD and indicate WM lesions were also an important cause of cognitive decline in AD.


2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Moses Q. Wilks ◽  
Hillary Protas ◽  
Mirwais Wardak ◽  
Vladimir Kepe ◽  
Gary W. Small ◽  
...  

We evaluate an automated approach to the cortical surface mapping (CSM) method of VOI analysis in PET. Although CSM has been previously shown to be successful, the process can be long and tedious. Here, we present an approach that removes these difficulties through the use of 3D image warping to a common space. We test this automated method using studies of FDDNP PET in Alzheimer's disease and mild cognitive impairment. For each subject, VOIs were created, through CSM, to extract regional PET data. After warping to the common space, a single set of CSM-generated VOIs was used to extract PET data from all subjects. The data extracted using a single set of VOIs outperformed the manual approach in classifying AD patients from MCIs and controls. This suggests that this automated method can remove variance in measurements of PET data and can facilitate accurate, high-throughput image analysis.


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