Molecular Pathways and the Interaction with Naturopathic Medicine
Neurodegenerative diseases are linked to the synthesis of insufficient neurotransmitters and abnormal ubiquitination (Morris et al. 941). Alzheimer’s disease (AD) is characterized by death of neurons. The main feature of AD is the aggregation of β-amyloid (Aβ). The aggregation leads to oxidative stress characterized by antioxidant factors that result in reactive oxygen species (ROS) accumulation. The predominant loss of neurons in the AD is apoptosis pathway (Morris et al. 942). The pathway is further categorized into two pathways; intrinsic and extrinsic.
The intrinsic pathway is also called the mitochondrial pathway. In the pathway, the mitochondrion is acted on directly by stimuli. In the action, Bcl-2 family is affected. The principal constituents of Bcl-2 are the pro-apoptotic and anti-apoptotic proteins. Reduction in anti-apoptotic protein and subsequent rise in the pro-apoptotic proteins cause mitochondrial membrane destruction (Rezai et al. 178). The mitochondrial membrane swells and releases cytochrome c to cytoplasm. The action cleaves the procaspase; hence, initiation caspase cascades that causes the neuron death. The extrinsic pathway entails interaction of death signals. An example of the intrinsic pathway is the interaction of death receptors with tumor necrosis factor. The process forms death inducible that consequently activates caspase-8 (Rezai et al. 178).
In the two pathways death substrates, polymerase and ploy are activated by the caspase. In addition to the two distinct pathways, folding of proteins is affected by stress conditions in the endoplasmic reticulum. Endoplasmic reticulum takes place in three pathways that entail the folding of proteins. The activating transcription factor 6, Inositol-requiring enzyme 1 and protein kinase. There is no established curative or preventive therapy for AD. However, application of natural therapies to prohibit the process of the pathways can slow the progress of AD. The natural therapies include the medicinal plants that have compounds with a protective effect against Aβ. In addition, proteins, vitamins, and minerals that allow natural regeneration of neurons play a critical role in the onset and progression of AD (Jicha 49).
The omega-3 fatty acids play a vital role in the development of the brain. Polyunsaturated fatty acids facilitate incorporation of proteins bound membranes for the formation of lipid raft (Jicha 49). The amyloidogenic processing is influenced by omega-3 polyunsaturated fatty acid. The omega 3 polyunsaturated fatty acids activate α-secretase to produce fragments that that are not toxic; hence, inhibiting the formation of Aβ. The omega 3 polyunsaturated fatty acids influence the amyloidogen. In a controlled study in the Chicago Housing and Aging Project, a group of elderly was put to eat fish once a week or more while the control group did not take fish. The group eating fish was found to have 60% reduced risk of AD. There were no follow-up studies to determine the reason for the differences in the risk. Omega 3-polyusaturated fatty acids abundantly found in fish were pointed as the source of the difference (Morris et al. 943).
Molecular Techniques Used to Derive Data
Genomic technologies and biological information have increased. The genomic technique entails the analysis of DNA sequence to map the genes of animals, humans and microorganisms (Tanzi &Lars 183). The current techniques provide a basis in which pluripotent stem cells (iPSCs) are derived from the patients suffering from AD. Hossini et al. (3) conducted a study in which iPSCs was generated from patients with AD and from a control group. The fibroblasts were age-matched from control and AD patients that had ApoE3/E4 genotypes. The control group included two females aged 43 and 71 years. The iPSCs for the AD group (AD-iPSCs) included a female-aged 79 who had late onset of AD, a 47-year-old male with early onset of AD.
The genes associated with regions of the brain were found in the AD-iPSCs.
Therefore, the findings indicate that iPSCs molecular model represents a technique that provides data for neuronal disorders (Hossini et al. 3). During the study, the AD-iPSCs had expression pattern of genes associated with AD.
Impact of Naturopathic Medicine in a Neurodegenerative Disorder
The main features of neurodegenerative diseases are the oxidative stress followed by the depletion of antioxidants (Rezai et al. 182). Depletion of the antioxidants and the oxidative stress damages lipids, proteins, DNA and important biomolecules. The antioxidant effect of vitamin E inhibits oxidative stress. Vitamin E scavenges Aβ free radicals. The effect slows the progression of AD. However, Hu (11) noted that there is no sufficient evidence relating to the efficacy of vitamin E in the prevention of AD. Hu (4) noted that patients taking the vitamins experienced slow progression of Alzheimer’s disease. Hu (3) pointed that components such as the n-3 fatty acids, antioxidants and B-vitamins help in reducing the development of AD. For example, vitamin A and β-carotene have the ability to prevent the formation of fibrils and Aβ ologomers. The anti-ologomerization plays a crucial role in delaying the onset of AD. According to Hu (4), the plasma levels of both vitamin A and β-carotene are relatively low in patients suffering from AD. In addition, in vitro and vivo studies have found that vitamin C reduced the formation of Aβ ologomers.
Selenium plays a role in the anti-oxidative defense. Selenium has possible role in the prevention of AD onset. Patients suffering from AD have lower selenium plasma compared to the control groups. Metals such as copper, iron and zinc have a pathogenesis role of AD (Hu 13). They slow progression of AD by forming reactive species that are anti-AD development.
Genetic Factors and Recent Discovery
AD is caused by progressive collapse of brain cells. Jicha (46) noted that AD develops due to a multiplicity of factors. Therefore, there is no single identifiable cause of AD. The risk of AD increases to 50% as the age increases over 65 years. However, Tanzi and Lars (182) noted that AD is not a process of growing old. People from families that a parent or sibling has AD are at high risk of developing AD.
In the study of the family history and the relation to AD, Tanzi and Lars (182) found that the genes of influence included deterministic genes and risk genes. The presence of the genes increased AD risk (Tanzi & Lars 183). However, it is not absolute that the existence of the risk gene leads to AD (Tanzi &Lars 182). The common risk gene is the APOE-04; other risk genes are APE-e3 and APOE-e2. APOE gene is inherited from the parents. The people who inherit, the type APOE-e4 are at higher risk of AD. The deterministic genes have a direct cause of AD. Therefore, any individual who inherits the gene will certainly develop AD (Tanzi &Lars 182). According to Tanzi and Lars (182), few family genes cause AD. The genes associated with AD trigger production of B-amyloid.
Works Cited
Hossini, Amir et al. ‘Induced pluripotent stem cell-derived neuronal cells from a sporadic Alzheimer’s disease donor as a model for investigating AD-associated gene regulatory networks.’ BMC Genomics, 16.1 (2015): 2-15. Print.
Hu, Nan et al. ‘Nutrition and the Risk of Alzheimer’s Disease.’ Biomed Research International, 2013.1 (2013): 1-15. Print.
Jicha, Gregory. ‘Omega-3 fatty acids: potential role in the management of early Alzheimer’s disease.’ Clinical Intervention in Aging, 5.1 (2010): 45–61. Print.
Morris, Bienias et al. ‘Consumption of fish and n-3 fatty acids and risk of incident Alzheimer disease.’ Arch Neurology Journal, 60.7 (2003): 940–946. Print.
Rezai, Zadeh et al. ‘Green tea epigallocatechin-3-gallate (EGCG) reduces beta-amyloid mediated cognitive impairment and modulates tau pathology in Alzheimer transgenic mice.’ Brain Research, 1214.1 (2008): 177–187. Print.
Tanzi, Rudolph E., and Lars Bertram. ‘New frontiers in Alzheimer’s disease genetics.’ Neuron, 32.2 (2001): 181-184. Print.