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Role of Vitamin D and Antioxidants in the Prevention and Treatment of Alzheimer’s Disease
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Shilia Jacob Kurian, Ruby Benson, Sonal Sekhar Miraj, Mahadev Rao
Some studies do report alternative outcomes; in this situation, it is interesting to consider apolipoprotein E ε4 (APOE-ε4) genotype and the overall dietary habits. For instance, APOE ε4 carriers may have increased serum vitamin D levels owing to enhanced intestinal absorption and reduced renal excretion of vitamin D. A study found the association among APOE-ε4, serum vitamin D, and AD, and proposed a significant relationship among these three factors (Dursun et al. 2016). They further concluded that vitamin D deficiency (VDD) is more prevalent in AD patients who are noncarriers of APOE-ε4, thereby indicating proper screening of VDD in AD patients (Feart et al. 2017; Dursun et al. 2016).
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).
Current Research on Alzheimer’s Disease In a Historical Perspective
Published in Zaven S. Khachaturian, Teresa S. Radebaugh, Alzheimer’s Disease, 2019
Another provocative finding, obtained in one longitudinal study that included cardiovascular as well as neurological workups on a yearly basis, the Bronx Aging Study, is that myocardial infarct is a risk factor in elderly women. This finding takes on added interest in view of the finding that the Apolipoprotein E4 allele is a risk factor for both heart disease and Alzheimer’s disease. This finding has yet to be confirmed in other studies. However, Sparks et al.61 have reported a very significant increase in plaques in neocortex in medical examiner cases of elderly individuals who had a 75% stenosis of a coronary vessel compared to those who did not have heart disease.
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].
Novel biomarkers in Alzheimer’s disease using high resolution proteomics and metabolomics: miRNAS, proteins and metabolites
Published in Critical Reviews in Clinical Laboratory Sciences, 2021
Diana Navas-Carrillo, José Miguel Rivera-Caravaca, Arturo Sampedro-Andrada, Esteban Orenes-Piñero
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder affecting almost 50 million people around the world. It is the most common cause of dementia worldwide [1]. AD is characterized by two landmark pathologies, extracellular senile plaques consisting of amyloid-beta (Aβ) peptides and intracellular neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau proteins [2]. As the disease progresses, amyloid and neurofibrillary proteins accumulate in localized areas of the brain, forming plaques and tangles that disrupt neuronal signaling and ultimately lead to the loss of neurons and brain tissue [3]. These features result in loss of neurogenesis and synaptic plasticity in the hippocampus, the main region of the brain involved in regulation of cognition and memory [4]. The pathogenesis is also associated with a deficit in multiple neurotransmitters, including cholinergic markers, choline acetyltransferase and acetylcholinesterase, as well as deficiencies of serotonin, noradrenalin, somatostatin and corticotrophin-releasing factors [5]. Apolipoprotein E4 alleles are involved in the predisposition to develop the disease [6]. Therefore, it can be said that whilst the etiology of AD is still somewhat dubious, it is recognized as an interaction between genetic and environmental factors.
Factors influencing recovery from mild traumatic brain injury
Published in Brain Injury, 2020
Leslie Weaver Johnson, Kristine Lundgren, Vincent Henrich, Susan Phillips
Recently, researchers have begun to examine the potential role of genetics in determining functional outcome after TBI. Specifically, investigators have studied the role of apolipoprotein E (APOE) on cognitive recovery and long-term functional outcome (19). The APOE gene provides instructions for making a protein called apolipoprotein E (apoE). This protein combines with fats in the body to form molecules called lipoproteins which the brain uses to maintain, restore, and/or stabilize its synaptic connections, otherwise known as plasticity (20). This plasticity is likely a key contributor in the rehabilitation process after brain injury. In its normal functioning, apoE does not cross the blood-brain barrier. However, in response to injury, the apoE protein may positively influence the central nervous system by acting as an anti-excitotoxic, antioxidant, and/or anti-inflammatory agent (14).