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Phytotherapeutic Potential For the Treatment of Alzheimer’s Disease
Published in Atanu Bhattacharjee, Akula Ramakrishna, Magisetty Obulesu, Phytomedicine and Alzheimer’s Disease, 2020
Muhammad Akram, Atanu Bhattacharjee, Naveed Munir, Naheed Akhter, Fozia Anjum, Abida Parveen, Samreen Gul Khan, Muhammad Daniyal, Muhammad Riaz, Fahad Said Khan, Rumaisa Ansari, Umme Laila
Apolipoprotein E is also a causative agent in the development of AD. Different form of apolipoprotein E are present, like apolipoproteins E2, 3, and 4. Glial cells of the brain, which are also called astrocytes, produce these proteins. The risk of developing AD is greater in the presence of higher apolipoprotein E4 concentrations (Aaronson, Van Den Eeden et al. 2017). If the level of this protein increases, then the probability of death is also increased (Harris, Brecht et al. 2003). AD is also associated with E693G mutations in a gene encoding an amyloid precursor protein (Nilsberth, Westlind-Danielsson et al. 2001). Furthermore, AD is caused by oxidative stress because, in this situation, demand by the brain for oxygen is increased (Butterfield and Lauderback 2002). AD is also associated with some pathogens like Chlamydia pneumoniae, which enter the brain tissue and damage brain cells (Harris, Brecht et al. 2003). AD is more common in females, smokers, obese people, patients with high blood pressure or a high level of cholesterol, whereas previous trauma, changes in sleep pattern, and Down syndrome can all increase the risk of AD (Simonson 2018).
Clinical Assessment of Patients with Dementia
Published in Zaven S. Khachaturian, Teresa S. Radebaugh, Alzheimer’s Disease, 2019
A history of cognitive and movement disorders in parents and siblings is an important aspect of the evaluation since many dementias are either clearly hereditary or strongly influenced by genetic factors. Many kindreds of Alzheimer’s disease with autosomal dominant inheritance have been described, with loci on chromosomes 14,19, and 21.15-20 Many of these clearly inherited cases develop cognitive disorders at a relatively young age. Moreover, family studies of older-onset Alzheimer’s disease indicate that by age 90 years, approximately 50% of the first-degree relatives of people with dementia will become demented themselves.21,22 Recent studies indicate an association between the E4 allele of apolipoprotein E (APOE) and both familial and sporadic forms of late-onset Alzheimer’s disease.23
Amyloid beta and tau proteins in Alzheimer’s disease and Down syndrome
Published in Vee P. Prasher, Down Syndrome and Alzheimer’s Disease, 2018
Apolipoprotein E (ApoE) is a 34-kDa polymorphic protein that is involved in the transport and redistribution of lipids among various tissues. ApoE occurs as three major isoforms (E2, E3 and E4) and is encoded by three alleles (ϵ2, ϵ3 and ϵ4) at the ApoE locus on chromosome 19. The ApoE ϵ4 allele is a significant risk factor for the development of sporadic and familial late-onset DAD.4,5
Posterior cortical atrophy: clinical, neuroimaging, and neuropathological features
Published in Expert Review of Neurotherapeutics, 2023
John Best, Marianne Chapleau, Gil D. Rabinovici
PCA is currently considered more of a sporadic than inherited syndrome, as the syndrome is rare in autosomal dominant cases of AD. To date, there are no clear causative genes, although with the majority of cases due to underlying Alzheimer’s disease, there is an overlapping genetic risk profile with typical Alzheimer’s disease. An exploratory genome-wide association study (GWAS) identified a number of possible risk genes. Similar to typical Alzheimer’s disease, the apolipoprotein E ε4 genotype (APOE ε4) was associated with an increased risk of PCA (odds ratio 2.03) but to a lesser extent than the associated risk with typical AD (OR 2.83) [12]. Other putative risk alleles for both typical AD and PCA include variants in CR1 (a complement receptor), ABCA7 (ATP binding cassette transporter), and BIN1 (adaptor protein which may be involved in synaptic vesicle endocytosis) [12]. Potential associations with PCA, but not typical AD, were identified with the genes SEMA3C, CNTNAP5, and FAM46A. SEMA3C is a chemotrophic molecule involved in cortical axon development and has been shown to influence the development of the visual system. CNTNAP5 is involved in cell adhesion and intercellular communication and has previously been identified as a risk factor for bipolar and autism spectrum disorder. FAM46A is expressed in the retina and implicated in retinal degenerative pathways [5].
Amyloid nomenclature 2022: update, novel proteins, and recommendations by the International Society of Amyloidosis (ISA) Nomenclature Committee
Published in Amyloid, 2022
Joel N. Buxbaum, Angela Dispenzieri, David S. Eisenberg, Marcus Fändrich, Giampaolo Merlini, Maria J. M. Saraiva, Yoshiki Sekijima, Per Westermark
Amyloid deposits not only contain the main amyloid fibril proteins but may also have components that appear to be present in most deposits. The most well studied are serum amyloid P-component (SAP) and heparan sulphate proteoglycans (HSPG), both of which seem to be important both for the stability of the fibrils and, at least for HSPG, in their genesis. There are other proteins regularly found attached to the fibril by uncertain mechanisms. They include among others, apolipoprotein A-IV and apolipoprotein E; with other components under continuing investigation. The presence of these proteins has been used in mass spectrometry as additional proof that the tissue extracted material contains amyloid. Therefore, these components have been designated as ‘amyloid signature proteins’ [6].
Prevalence of candidate single nucleotide polymorphisms on p53, IL-11, IL-10, VEGF and APOE in patients with repeated implantation failure (RIF) and pregnancy loss (RPL)
Published in Human Fertility, 2020
Azahara Turienzo, Belén Lledó, José A. Ortiz, Ruth Morales, Juan Sanz, Joaquín Llácer, Rafael Bernabeu
Finally, other proteins that are not major players might also affect the correct implantation and development of the pregnancy. For example, apolipoprotein E (APOE) is involved in the transport of lipoproteins, lipid soluble vitamins and cholesterol into the lymphatic system and subsequently into the bloodstream (Mahley, Weisgraber, & Huang, 2009). A deficient protein could produce lipid accumulation in the bloodstream increasing thrombotic risk. The ApoE (19q13) gene consists of four exons. It has three polymorphic isoforms: ApoE E2 (cys 112, cys 158), ApoE E3 (cys 112, arg 158) and ApoE E4 (arg 112, arg 158) that produce six different genotypes: E2/E2, E2/E3, E2/E4, E3/E3, E3/E4 and E4/E4. Different genotypes have been associated with reproductive problems mainly RPL (Li, Chen, Wu, & Li, 2014).