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What Causes Death In Alzheimer's Patients

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What Causes Death In Alzheimer's Patients

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By Ujala Sehar Ujala Sehar Scilit Preprints.org Google Scholar 1, Priyanka Rawat Priyanka Rawat Scilit Preprints.org Google Scholar 1, Arubala P. Reddy Arubala P. Reddy Scilit Preprints.org Google Scholar 2, Jonathan Kopel Jonathan Kopel Scilit Preprints . Scholar 1 and P. Hemachandra Reddy P. Hemachandra Reddy Scilit Preprints.org Google Scholar 1, 2, 3, 4, 5, *

Department of Biomedical Sciences, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA

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Department of Speech, Language and Hearing Sciences, School of Health Sciences, Texas Tech University Health Sciences Center, Lubbock, TX 79430, USA

Received: 28 September 2022 / Revised: 18 October 2022 / Accepted: 24 October 2022 / Published: 26 October 2022

Alzheimer’s disease (AD), is a progressive neurodegenerative disease that affects behavior, thinking, learning, and memory in the elderly. AD occurs in two forms, familial onset and late onset; Genetic mutations in the PS1, PS2, and APP genes cause early-onset familial AD, and a combination of lifestyle, environmental, and genetic factors predispose to early-onset AD. . However, rapid disease progression is observed in patients with familial AD. Pathological changes are synaptic damage, and changes in mitochondrial production and function, in addition to increased production and accumulation of phosphorylated tau (p-tau), and amyloid beta (Aβ) in the affected brain areas. in AD patients. Aβ is a peptide derived from the amyloid precursor protein (APP) by proteolytic cleavage of beta and secreted proteins. APP is a glycoprotein that plays important roles in maintaining neuronal homeostasis such as signaling, neuronal growth, and cell transport. Aβ has been reported to have both protective and toxic effects on neurons. The purpose of our article is to summarize the recent development of Aβ and its association with synapses, mitochondria, microglia, astrocytes, and its relationship with p-tau. Our article also covers therapeutic strategies that reduce Aβ toxicity and disease progression and discusses the reasons for failure of Aβ therapy.

Alzheimer’s disease (AD), is a neurodegenerative disease, which is characterized by memory loss and many other brain disorders. AD is associated with cognitive decline and is the fourth leading cause of death worldwide among the elderly [1]. AD causes progressive impairment and death of neurons, so AD patients tend to lose their cognitive and memory abilities [2]. It has been found that vivid and vivid memory is affected in AD patients, which means that the disease affects a person’s ability to remember recently processed information/events, and it also affects such as reinforcement, performance depends on previous experience or training [3]. . . AD comes in two forms, familial early AD, and early-onset AD, and memory disturbances are more common in early-onset patients compared to late-onset patients.

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Several modifiable and non-modifiable risk factors are associated with AD (Figure 1). Modifiable risk factors include type 2 diabetes, obesity, vascular disease, stroke, depression, brain injury, and many lifestyle factors, while non-modifiable risk factors may include genetic morphisms, age, or sex [5]. Early detection and diagnosis is very important for AD, because this disease is a public health concern in the United States, according to estimates, 6.5 million Americans currently have AD [6]. Alzheimer’s Disease International, the umbrella of more than 100 Alzheimer’s diseases, estimates that up to 60 million people in the world suffer from dementia, and this number will reach 78 million in 2030. [7]. Worldwide, the number of deaths from dementia has been increasing rapidly since the 1990s, the death rate has increased from 10.49 deaths per 100,000 to 20.98 deaths per 100,000 from 1990 to 2019 [8].

According to World Health Organization data, Finland is the country with the highest death rate from dementia with 56.65 deaths per 100,000 [9]. The top 10 countries with the highest death rates due to dementia are shown in Figure 2. The global economic burden of AD and related dementias is estimated at $2.8 trillion in 2019. , we predict and will increase to $ 4.7 trillion from. . 2030. Furthermore, low- and middle-income countries are expected to account for 65% of the world’s economic burden of AD in 2050 [10].

Some of the main clinical features of AD are memory loss, cognitive impairment, and behavioral changes [11]. Selective memory impairment is often the first symptom of AD but there is no cure for this disease, only treatments aimed at reducing symptoms [12]. Pathological factors include the formation of neurofibrillary tangles (NFTs) consisting of abnormal aggregation of phosphorylated tau protein and the development of adult plaques from amyloid beta in the hippocampus [11]. Aβ is a peptide derived from the precursor amyloid protein by proteolytic cleavage. APP is a glycoprotein that plays an important role in maintaining neuronal homeostasis such as signaling, neuronal growth, and intracellular transport [13]. Tau protein is a microtubule-associated protein and is found abundantly in neurons of the central nervous system (CNS) that is involved in the stability of microtubules and axons but is also important for synaptic plasticity, the process of stability genomic, and expression cells. [14]. Along with the interaction of these proteins, many other health, lifestyle, and environmental factors are responsible for AD.

The purpose of our article is to provide the most recent and relevant research on the structure, function, interaction, and treatment of amyloid beta.

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Genetic and non-genetic factors are believed to cause AD, but the etiology of the disease is unknown. Although genetic factors such as mutations in APP, PSEN1 and PSE2 are known to be inherited in a non-genetic Mendelian pattern such as functional exposure to volatile anesthetics, pesticides, industrial chemicals, electromagnetic fields , air pollution, and pesticides in the environment. decide. Furthermore, some existing medical conditions such as diabetes, cerebrovascular disease, hypertension, cancer, depression, brain injury, and dyslipidemia may also be responsible for the etiopathogenesis of AD (Figure 1). Lifestyle habits such as caffeine consumption, and alcohol consumption, physical activity, mental exercise, and physical activity are also important factors [15].

Any long-term exposure to the environmental pollution mentioned above can lead to the bioaccumulation of toxins in human life and can cause neuropathology and neuroinflammation that cause the development of AD, however, knowledge of the association and – infection among those with the disease and prognosis of AD. have limits. However, studies on AD animal models have demonstrated the toxic effects of environmental pollution at the cellular level affecting metabolic pathways associated with AD [16]. One of the most well-studied factors is the Aβ protein which is a key component of the AD process [17]. Aβ accumulation is the first step of AD and accumulation begins in the entorhinal cortex and hippocampus of the brain. Furthermore, the hyperphosphorylated protein, tau, deposits intracellularly in neurofibrillary tangles that alter the cytoskeleton and inhibit axonal transport [18]. The concept of Aβ accumulation as a key factor in AD pathogenesis was presented by three independent research groups in 1991 [ 19 , 20 , 21 ].

In AD patients, the digestion of APP occurs by a combination of alpha- and gamma-secretases that produce insoluble peptides, amyloid-beta, which aggregate to form amyloid beta plaques and destroy cells [22]. In a healthy brain, Aβ is broken down by beta-secretase enzymes that produce soluble APP fragments, and other APPs are broken down by γ-secretase peptides that are taken outside the cell and quickly removed/ degraded. . However, in adults, secretase homeostasis is dysregulated, and APP is cleaved by β and γ-secretase and produces insoluble amyloid beta peptides [23].

The APP gene in humans is located on chromosome 21 and further deletion of the gene produces 8-11 isoforms.

Alzheimer’s Disease Facts And Figures

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