Most Common Cause Of Alzheimer's Disease (AD)

Alzheimer 's disease (AD) was discovered by a German doctor Alois Alzheimer in 1906 when he found amyloid plaques and neurofibrillary tangles in the autopsy of a woman who died of an unknown mental disease. The extracellular amyloid plaque deposits, composed of insoluble amyloid-Beta peptide were hypothesized to be the main etiological factor. “The most important abnormality is an excess of Amyloid-beta peptides brought about through either overproduction or failure in degradation.” (Uzun, Kozumplik, & Folnegović-Smalc, 2011) Later, it was discovered that intracellular neurofibrillary tangles composed of hyper-phosphorylated, helically-paired tau

Alzheimer’s disease (AD) is a form of dementia that causes problems with memory, thinking, and behavior. AD typically involves the development of a progressive neuropsychiatric disorder that is characterized by gradual memory impairment, loss of acquired skills and emotional disturbances (Lee, Y. J., Han, S. B., Nam, S. Y., Oh, K. W., & Hong, J. T.). Every 67 seconds an individual in the United States develops AD. AD is the sixth leading cause of death in the United States. There are 5.3 million Americans diagnosed with AD (Latest Alzheimer's Facts and Figures). AD is one of the few degenerative diseases that cannot be prevented, stopped, or cured (Latest Alzheimer's Facts and Figures). Post-mortem examination of the brain of AD patients usually

Alzheimer’s disease or AD is an incurable disorder of the brain that results in loss of normal brain structure and function. In an AD brain, normal brain tissue is slowly replaced by structures called plaques and neurofibrillary tangles. The plaques represent a naturally occurring sticky protein called beta amyloid and in an Alzheimer’s brain, sufferer’s tend to accumulate too much of this protein. Neurofibrillary tangles represent collapsed tau proteins which, in a normal brain along with microtubules, form a skeleton that maintains the shape of the nerve cells. In Alzheimer’s disease, the tau proteins break loose from their normal location and form tangles. Without the support of these molecules, nerve cells collapse and die. As normal

Under normal condition tau binds to microtubules, stabilizing neuronal structure and integrity. Hyperphosphorylation of tau is assumed to be the cause of the formation of paired helical filaments - neurofibrillary tangles (NFT). The principle components of the senile plaques are neurofibrillary tangles in the cell bodies, neuropil threads, and neurites as well as extracellular A-beta amyloid. These lesions are surrounded by microglial and astrocytes. The brain regions affected by Alzheimer’s disease also contain neuritic or senile plaques in which extracellular deposits of amyloid are surrounded by dystrophic axons as well as the process of astrocytes and microglia. The principle constituent of amyloid is a 4kDa peptide called A-beta amyloid. A-beta amyloid is cleaved from a larger precursor protein called amyloid precursor protein. Similar abnormalities occur in transgenic mice with mutant APP and in individuals with Alzheimer’s

Alzheimer’s disease (AD) is a slow-progressing neurodegenerative disease that has no cure and most often affects people over the age of sixty-five. Neurodegeneration is characterized by the loss of function in the central nervous system due to degeneration of neurons found mostly in the brain. The most recent data from the Center for Disease Control and Prevention shows that AD is the sixth-leading cause of death in the United States. The cause of Alzheimer’s is still not completely understood, but the current theory is that it appears to be genetic in which many genes are involved. AD is also the most common form of dementia and accounts for 60-80% of cases (Alzheimer’s Association 2016). Dementia is not a disease itself, but instead is characterized by a group of symptoms that is caused by brain disease or injury in which memory, personality, and reasoning skills are affected.

Alzheimer’s is a disease which affects the brain. Being completely irreversible, a person’s memory, thought process, and motor skills become drastically challenged, and eventually taken away. Symptoms will usually appear in subjects around age 60, however, signs have been known to start much earlier. Drastic changes can also occur with the brain, visibly shrinkage occurs, and neurons slowly cut off from each other, and die. In addition to this, unnatural formations of proteins begin forming on the brain. (ADFS)

Main reason for cognition decline could be buildup of plaque and dysfunctional proteins in the brain interfering with neuronal function. Alzheimer’s disease (AD) is an age-related neurodegenerative disease that accounts for more than 60 % of all dementia cases. The disease is characterized by cognitive deficits and memory loss through a process that lead to the presence of amyloid-β (Aβ) plaques and neurofibrillary tangles (NFTs). This plaque is composed of abnormally hyperphosphorylated tau protein in the brain. Amyloid beta (Aβ or Abeta) is a peptide of 36–43 amino acids, forms amyloid plaques in the brain and are toxic to nerve cells. These peptides result from the amyloid precursor protein (APP), which is cleaved

All the neurons work together like a tiny community; different groups take in information, produce energy, assemble equipment, and dispose of waste. In order for this “community” to run smoothly, the cells need to be able to handle and store information, and most importantly, correspond with other cells. Alzheimer's inhibits these cells from performing like the community; when cells incapable of carrying out their jobs, they die and cause permanent impairment to the brain. The suspected “culprits” are tangles and plaques. Plaques are accumulations of a protein particle known as beta-amyloid; these deposits concentrate in the spaces between brain cells. Tangles are contorted fibers of a different protein called tau, that collect inside the nerve cells. Plaques and tangles cut off communication among cells, thus hindering the “community” and killing

“Alzheimer’s disease is an irreversible, progressive brain disorder that slowly destroys memory and thinking skills, and eventually the ability to carry out the simplest tasks individuals with AD may start having symptoms their mid-60s” (nih.gov). AD is a multifactorial and progressive neurodegenerative disease. “Parts of AD, for example, increased oxidative state, amyloid plaque deposition, and neurofibrillary tangle of tau protein in the central cortex the limbic system of the brain, have been related with Alzheimer 's disease. The disease was once thought to be a natural part of aging; it is an extremely incapacitating type of mental dementia. Albeit, some dementia

According to Sadigh et al (2015), AD occurs when the dysregulation of the amyloid-beta (Aβ) levels leads to the appearance of senile plaques, which contain Aβ depositions. Aβ is a complex biological molecule that interacts with many types of receptors and forms

Alzheimer’s disease is a neurodegenerative disorder, it affects two pathological hallmarks: amyloid plaques and neurofibrillary tangles. “Amyloid plaques are caused when protein pieces called beta amyloid stick together, they eventually build up between the nerve cells into plaques.” (Ballard, 2011) Amyloid plaques trigger neurological dysfunction and eventually brain death. Compared to a healthy brain the amyloid is broken down and disposed, however in AD they collect and form hard plaques. “Once brain death happens there is no way for the brain to communicate, or restore memory” (Brightfocus.org, 2014). Neurofibrillary tangles are fibers found in the brain cells, and they have a primary protein called ‘tau’ which aids in the structure called microtubule. “Microtubules help move nutrients and other factors from one cell to another with Alzheimer’ the ‘tau’ protein is abnormal and the microtubule structure collapses.” (Ballard, 2014 & Brightfocus.org, 2014) Even though we often see the effects of AD on the outside; it is a neurodegenerative disease effecting the amyloid plaques and

The fact that AD usually develops later in life again complicates the boundaries of this disease. Because the process of normal aging is not completely understood, there are no consistent, established values of what constitutes "normal" cognitive impairment and memory loss with advancing years. Furthermore, the neurochemical changes, the neurophysiological changes, or the gross and fine anatomical changes that accompany normal aging are not understood well enough to provide a firm basis for determining "abnormal" changes. The brain of an 80 year old patient with AD may be difficult to distinguish from that of an age-matched normal patient without dementia. Also, some elderly patients have few or no senile plaques or neurofibrillary tangles. Even at earlier ages, the neurofibrillary tangles and senile plaques that

Alzheimer’s disease is among the sixth top leading causes of death in the United States and even with an estimated 4.5 to 5.4 million suffering from Alzheimer’s disease (AD) not much is known about the causes. Only the symptoms are addressed. The main characteristics of AD are degeneration of the ability to remember, reason, communicate and with loss of motor skills and function (Piazza-Gardner, 2013). Cognitive function that is lost and is accompanied by other physiological conditions such as depression, anxiety, irritability, aggression and inappropriate behavior for a setting or location that occur in most AD suffers (Senie, 2014). AD was noted as abnormal clumps and a bundle of proteins in the brain which was discover in patients with

Both tangles and amyloid protein lead to cognitive impairment due to neuronal death. These also affect neural transmission. Amyloid protein and tangles kill off the healthy neurons. By killing off these neurons, the brain then shrinks in size. Alzheimer’s disease is also hard to deal with psychologically. Losing the ability to remember events, people and how to live in daily life takes a huge toll on the patient’s psychology. Alzheimer’s is often referred to as an “end-of-life issue” because of the deterioration of the brain. Due to the neurons and neurotransmitters in our brain, it is highly likely that depression is the result of the brain shrinkage. It is expected that once diagnosed with AD, depressive symptoms will arise from the patient and if not the patient, than the caregiver.

The amyloid cascade hypothesis is the most widely accepted of the AD pathogenesis hypotheses. Its principle is that the accumulation of Aβ plays a major role in AD pathogenesis, and the disease is analyzed as a series of abnormalities in the process and secretion of the amyloid precursor protein (APP), where an inequality between production and clearance of amyloid β is the triggering event and the most important factor responsible for other abnormalities observed in AD (Hardy et al, 2002; Cummings et al, 2007). Amyloid β is a peptide with high resistance to proteolytic degradation. It consists of 37–43 amino acids with different isoforms (Deane et al, 2009). Aβ is the result of sequential cleavage of the amyloid precursor protein (APP), generating