The Role Of Oxidative Stress In Alzheimer's Disease

INTRODUCTION Alzheimer’s Disease has been one of the top leading causes of death in our country. It is understood that this disease is identified as an excess of the protein amyloid-ß within an increase of plaque (Seneff, Wainwright, and Mascitelli, 2010). Additionally, as the brain ages, it gets used to the

Abstract: According to data available from the Alzheimer’s foundation every 67 seconds someone develops Alzheimer’s disease and currently at least 5.3 million people are affected by the disease. The numbers are expected to grow as 75 million baby boomers transition into retirement by 2030. Alzheimer disease is a brain disorder that causes decay and dis- function of neurons resulting in memory loss, speech and language impairment. This can also extend to challenges in physical and social behavioural. The brain, consisting of the cerebrum, cerebellum and brain stem is the primary target of Alzheimer’s disease. At three pounds the brain has a network of arteries and a folded cortex that is responsible for memory and movement. These functions are facilitated by a network of neurons. Alzheimer’s disease interferes with these neurons by disrupting electrical transfer; Death of brain cells is inevitable as the cortex shrinks becoming incapable of developing thoughts and memory. The Alzheimer’s patient experiences an altered personality with family members becoming strangers.

AD is a progressive age-related neurodegenerative disorder that poses increasing challenges to the global healthcare system and economic development. AD is characterized by extracellular neurotic plaques composed of Aβ deposits and intracellular neurofibrillary tangles composed of hyperphosphorylated tau with progressive loss of synapses in the brain [1]. Evidence demonstrates a potential link between oxidative stress, mitochondrial dysfunction and AD development [2]. Oxidative damage has been known to occur at a very early stage of AD even prior to Aβ plaque formation and the onset of symptoms [3, 4, 5]. Several cellular changes by oxidative stresses have been related with Aβ plaques formation and pathophysiological events of AD [6].

Dementia is a syndrome which is progressive in nature, characterized by impairment of memory and loss of intellectual ability.1 Decreased level of Acetylcholine in the brain, neuro-inflammatory reaction, rise in the oxidative stress and hypercholesterolemia have been reported to play an important etiological role in the memory decline.2 Alzheimer’s Disease (AD) is the most common form of dementia which is a progressive and a neurodegenerative disease characterized by the presence of senile plaques rich in insoluble aggregates of β amyloid and neurofibrillary tangles in the brain. AD has been estimated to account for 50–60% of dementia cases in persons over 65 years of age worldwide.3 Alzheimer’s Disease International

Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the most widespread age-related neurodegenerative diseases. Both diseases impact a considerable number of people, where AD occurs in around 10 percent of the population greater than the age of 65 while PD occurs in roughly 1 percent of the population above the age of 65. AD is considered to be the most widespread cause of dementia, characterised by the progressive memory and cognitive deficits which impair ones day to day activities. The pathological hallmark of AD comprises of extracellular accumulation of senile plaques consisting of mainly amyloid-beta (Aβ) peptides, along with neurofibrillary tangles which are composed of the phosphorylated tau protein, located in the hippocampus and cortex. Conversely, PD is considered to be the most widespread movement disorder that is characterised by symptoms such as rigidity slow movements, resting tremor and other instabilities. The extreme loss of dopaminergic neurones in the substantia nigra is what defines PD, as the loss of this nerve cell can be linked to Lewy bodies containing aggregates of a soluble protein called α-synuclein.

Last year my maternal Aunt Kate passed away. She had been diagnosed with Alzheimer’s disease (AD) about eight years earlier. My maternal grandmother also had been diagnosed with dementia before her death. Later this month I will accompany my 77-year-old mother to her neurologist appointment. While she has not been diagnosed with AD or dementia, she has been prescribed Donepezil (Aricept), one of the newer drugs that are thought to reduce the decline in memory in patients that have or might be developing dementia. I welcome opportunities to learn more about AD and the effects on the brain. The Alzheimer’s Association website, ALZ.org, is filled with a wealth of this information. Especially interesting was “Inside the Brain: An Interactive Tour.” I learned about changes the normal brain experiences from early, mild to moderate and severe stages of Alzheimer’s disease.

Awareness is necessary in understanding this disease. As humans continue to live longer, the risk for many illness and deficiencies begin to present them. Alzheimer’s and dementia is one of the many problems that plague the aging population. Understanding brain aging and reducing risk for neurological disease with age requires searching for mechanisms and treatment options beyond the age-related changes in neuronal

Last year my maternal Aunt Kate passed away. She had been diagnosed with Alzheimer’s disease (AD) about eight years earlier. My maternal grandmother also had been diagnosed with AD before her death. Later this month I will accompany my 77-year-old mother to her neurologist appointment. While she has not been diagnosed with AD, she has been prescribed Donepezil (Aricept), one of the newer drugs that are thought to reduce the decline in memory in patients that have or might be developing dementia. I welcome opportunities to learn more about AD and the effects on the brain. The Alzheimer’s Association website, ALZ.org, is filled with a wealth of this information. Especially interesting was “Inside the Brain: An Interactive Tour.” (Alzheimer 's Association, 2015). I learned about changes the normal brain experiences from early, mild to moderate and severe stages of Alzheimer’s disease.

Alzheimer’s disease (AD) has been ranked the third leading cause of death after heart disease and cancer. New research suggests the ways of

Alzheimer’s Disease accounts for sixty to seventy percent of dementia cases. The disease starts slowly and gets worse over time. The most common symptoms are short term memory loss, trouble with language , moods swings

Scientists believe that the combinations of genetics, environmental factors, and lifestyle play a huge part in Alzheimer’s disease. Scientists are learning that age-related changes may harm neurons. These changes include shrinking of the brain, and inflammation. In early-onset genetic mutation is usually the cause, and people thirty to sixty represent less than five percent of people with Alzheimer’s disease. In late-onset

Alzheimer’s disease (AD) is an incurable dementia illness characterized by chronic, progressive neurodegenerative Black has stated that genetic causes often involve the mutation of multiple genes and have identified at least five chromosomes: 1, 12, 14, 19, and 21 (Black, 2009, p. 1894). Four genetic loci have also been identified as contributing to AD, including the amyloid precursor gene, the presenilin 1 gene, the presenilin 2 gene, and the apolipoprotein E gene on chromosome 19. Though there is not enough conclusive research to directly link AD to environmental factors (such as toxins or head trauma) or personal health (diabetes, vascular disease, heart and stroke), these issues are known to contribute to the destruction of brain cells. Understanding the etiology of brain cell loss is relevant to understanding how to effectively prevent the loss of function in the brain. For example, preventing the formation of chemicals called free radicals with antioxidants can indirectly prevent AD. Other causes of brain cell loss include a neurotransmitter called glutamate and an accumulation of beta amyloid proteins. Therefore, although the cause of AD has been unidentifiable, many contributing factors have been observed.

Biology of Alzheimer’s Disease The evidence of neurofibrillary tangles is important to diagnosis. Inside the neurons, there will be abnormal clumps of tau protein. Tau protein normally attaches to microtubules of the neuron and acts as its stabilizer. Abnormal chemical changes cause Tau proteins to detach from the microtubules and stick to other tau proteins, forming threads, which clump together—tangles. Tangles may block the synaptic signaling between the neurons. Neurons will eventually begin to die and as this spreads, regions begin to shrink. The final stage will have widespread damage and significant shrinkage. Scientists are looking for specific types of cell death, which are found in normal aging, but greater in AD and the location matters. The brain will also show signs of inflammation in response to cellular injury (22, 23).

The News Article One of the most common forms of dementia in US is Alzheimer’s disease with an estimated 5.3 million Americans with Alzheimer’s disease in 2015 and approximately 700,000 patients of age 65 and older to die of this disease. Alzheimer’s has thus become the sixth leading cause of death

Introduction: According to the Alzheimer’s Foundation of America, Alzheimer’s disease is a disorder that results in memory loss, failed cognitive and language skills, and behavioral changes from progressive and degenerative damage on the brain’s neurons (Alzheimer’s Association of America, n.d.). The disease was first identified in the early nineteen hundreds by a German physician, Alois Alzheimer (Alzheimer’s Association, n.d.). Dr. Alzheimer’s began his research on the condition after a patient whom suffered from severe memory loss and psychological changes (Alzheimer’s Association, n.d.). The autopsy performed after the patient’s death led to the discovery of the disease (Alzheimer’s Association, n.d.). The causes, symptoms, and treatment methods for Alzheimer’s disease will be discussed in this paper.