The Structure Of Brain And Other Tissues Of Human Body Essay

Contrary to what many people believe, getting Alzheimer's is NOT a normal or natural part of aging. Yet, each year, there are more than 3 million people in the US diagnosed with Alzheimer's. Although, there is no real “cause” for this disease, factors that may contribute to it include age and family history, environmental components, particular genes (APOE-e4 or ADAD are the strongest risk genes), immune system complications, and protein deposits located in the brain. Therefore, since there is

At adult normal physiological condition, microglial display surveillance or so-called ‘resting’ phenotypes gauged by small cell body with extensively ramifying processes that actively surveying the CNS microenvironment. In this steady state, the turnover processes is primarily confined and well-maintained through local self-renewal of the long-lived resident microglial. Anomalies in the CNS such as infections, tissues damage, and accumulation of abnormal protein or biochemical can trigger microglial activation and in turn cause inflammation in CNS. Different from steady state, inflammatory condition may have disrupted the integrity of blood brain barrier and allowed recruitment of circulating myeloid cells and promotes their differentiation into microglial with more potent inflammatory properties and resulting heterogeneity of microglial . Activated microglial rapidly proliferate undergo phenotypic transition where they will exit from the ‘resting’ or ‘surveying’ form and mounted inflammatory effectors functions. Evidences showed that activated microglial capable of upregulated its phagocytose properties and secrete of inflammatory mediators chemokines, cytokines, nitrite, reactive oxygen species, and free radicals to execute repair

diabetes, chronic infections, inflammations, and hereditary. Aging People with diabetes are at a higher risk of developing Alzheimer’s disease (Marsa 54). Excessive brain specific insulin resistance impairments and signaling, account for many Alzheimer’s abnormalities. Brain insulin signaling regulates food intake, body weight, reproduction, also learning and memory. Defective insulin signaling results in cognitive ability decrease. Studies have also shown a link between chronic infections and inflammation in patients that develop Alzheimer’s disease. Viral and bacterial chronic infections, which cause cumulative damage, are an inflammatory vessel for Alzheimer’s disease. Infections have the potential to initiate a surge of events leading to inflammatory conditions of the central nervous system by generating free radicals and nitric oxide (Monastero et al. 107). There is an association between cognitive decline and systemic inflammation and infections. Successful treatment of chronic infections and inflammation is difficult but important in the effort of improving the quality of life in an Alzheimer’s patient. Alzheimer’s disease is not a normal part of aging; however, researchers know that genes play a part in the disease. There is a

Nevertheless, both types of AD are recognised pathologically by the build-up of intracellular neurofibrillary tangles, extracellular amyloid plaques, and massive neuronal and synaptic loss (Carmo & Cuello, 2013). Neurofibrillary tangles are aggregates of hyper-phosphorylated tau protein and plaques are mostly insoluble deposits of β-amyloid, resulting from the cutting of the amyloid precursor protein (APP) (Farooqui & Farooqui, 2011). The discovery of mutations in the APP gene which cause familial AD lead to the articulation of the amyloid cascade hypothesis (ACH) (Hardy & Asllop, 1991). A large amount of evidence supports this view; however a number of findings are contrary to its proposal. As a result, Armstrong (2011) proposed a revision of the hypothesis, postulating that the main trigger for the development of the disease is the ageing of the brain and related wear and tear such as head trauma and stress; collectively referred to as the “allostatic load” (Carroll, 2002). Furthermore, a greater emphasis has now been placed on the role of small, soluble amyloid oligomers which seem to be the cause of early cell dysfunction in AD, rather than the large, insoluble amyloid fibrils. (Ferreira, Vieira & De Felice, 2007).

The Aβ deposition and diffused plaque formation lead to local microglial activation, cytokine release, reactive astrocytosis and a multi-protein inflammatory response (Eikelenboom

Emerging evidence demonstrates neuroinflammation as a crucial pathophysiology of AD, specifically impacted by microglia and astroglia. 3 The microglia are distributed evenly across the brain and are activated by protein aggregation and neuronal cell death. 3 Specifically related to AD, the two chief proteins involved are amyloid-B and tau.3 An accumulation of microglia around amyloid-B plaques has been documented in post-mortem human brains and in animal models with AD.3 Research has yet to clearly determine if microglial activation plays a beneficial or detrimental role in the progression of AD..3 Some reports suggest that microglia are attracted to

Alzheimer’s Disease was first described over 100 years ago by Alois Alzheimer in Germany, characterising the first case with memory impairments and the presence of neuropathological plaques and tangles, which today, are major indications of the disease.² Progressive memory loss is the clinical trademark of AD but eventually, cognitive function also deteriorates.³ The neuropathological trademarks of AD involve the accumulation of β amyloid (Aβ) proteins expressed as plaques and the phosphorylation of tau proteins expressed as neurofibrillary tangles.³ The formation of these plaques and tangles are estimated to begin 20 years before clinical symptoms arise.² MRI studies have shown the association of AD with hippocampal atrophy, however, it remains difficult to distinguish from other forms of dementia.⁴

However, an essential role for systemic inflammation has been claimed also taking into account before listed data, traumatic brain injury and oxidative stress. Warning Signs of Alzheimer Disease: Changes in behavior and mood, Memory loss that mess up daily life, Experiments in planning or solving problems, Confusion with time or place, Difficulty completing familiar jobs, Losing things and losing the ability to review steps, difficulty in understanding visual images Problem with words in speaking or Writing, Removal from work or social

Since antibodies are not normally present in the CNS, microglial cells are the main active immune defense. As they are extremely plastic, microglia can adopt different morphologies, which two of the most important are the ramified and the activated one. The highly ramified morphology corresponds to the “resting” microglia, with long branches constantly moving and a small cellular body. The activated microglia presents a small amoeboid cell body with thicker and retracted branches, and it is associated with a pro-inflammatory phenotype. Microglial cells can go through the classical activation by stimulation with LPS and IFN-γ and can produce pro-inflammatory cytokines/mediators such as IL-1β, IL-6, TNF-α, CCL2, ROS, and NO18,19; suggesting that these molecules contribute to dysfunction of neural network in the CNS20. The microglia in this state is termed “M1 microglia”, while “M2 microglia” is used to include the states of both alternative activation21. IL-4 and IL-13 can induce alternative activation,

Alzheimer’s disease (AD) is one of the most widespread forms of dementia in the aging population. Unfortunately, most cases of AD are sporadic in nature and the underlying etiology is unknown. Thus far, the majority of the experiments have been based on transgenic mice models where amyloid aggregations are the causal initiator of AD. However, recent evidence has suggested that chronic inflammation may precede the induction of late-onset AD neuropathology. To demonstrate the role of neuroinflamamtion in late-onset development of AD, we injected a viral mimic polyinosinic:polycytidylic acid (polyI:C) to C57BL/6J pregnant mice during gestational day 17 (GD17). A subset of the pups were exposed to a second injection at 12 months of age to observe whether a second immune challenge would increase the rate of AD development. The aged mice were subjected to a cued fear-conditioning task to measure their cognitive capacity, and immunoblotting and immunohistochemistry to detect any neuropathological changes. PolyI:C injected mice failed to show any significant cognitive impairments following their

A journal article that was co-authored by Nancy Rothwell discussed the role of interleukin (IL-1) in inflammation of the brain leading to injury of the central nervous system (CNS) and disease. IL-1 is a cytokine

Neuroinflammation is also implicated with AD-related tau pathology (Yoshiyama et al., 2007). It’s been proposed that microglial activation can play a role in formation of NFTs (Metcalfe &

For those who don’t know, the brain is the most complex organ in the human body because of all the multiple sections that make up the brain. The human brain is found in the cranial cavity and is also a vital part of the nervous system. As a matter of fact, the reason why the brain is such a precious organ is because it allows us to interpret and store new information along with giving us the ability to move our body and enabling us to express ourselves.The brain can be broken up into three portions: the Forebrain, the Midbrain and the Hindbrain. These three potions regulate our body temperature, our breathing and heart rate as well as tell us when to eat and sleep. Therefore any severe damage to one of these portions could be life-threatening.

Pro-inflammatory changes lead to significant impairment in cognitive function in mouse models of AD {Heneka, 2002 #28}, {Heneka, 2006 #30}, {Jardanhazi-Kurutz, 2010 #38}, {Kalinin, 2007 #39} {Pugh, 2007 #69}. In addition, DSP4-mediated destruction of NE-ergic cells leads to decreased migration and phagocytosis by microglia and reduced colocalization between microglia and Aβ {Heneka, 2010 #29}. This suggests that a loss of NE-ergic cells could result in lower microglial cell function and a decrease in Aβ clearance in patients with AD. Indeed, DSP-4 injections in the Ts65Dn mouse model of DS has resulted in increased hippocampal inflammation and accelerated degeneration into AD-like pathology {Lockrow, 2011 #54}.

The brain is the greatest, the most fascinating and the most complex organ of the human been. According to Dr. Wolfe, the human brain weighs about three pound. Humans do not feel its weight because it is full of fluids and it is floating. The human brain consumes ten times more oxygen of all the humans’ body parts and 25% of the total energy produced by the body. It is not the largest part of the humans’ body, but it is one of the most important parts. Through the years educators were like doctors giving certain treatment to their patients without being sure what the disease was. If the first treatment given did not work they gave another treatment and so on. Nowadays technology has help to study how animals and humans brain works. It also has helped to discover how and where information is manipulated within the brain during the learning process. To discover how the brain works, the brain was divided in many parts. According to the book, the brain structures are cerebellum, brain stem, temporal lobe, broca’s area, frontal lobe, motor cortex, sensory cortex, parietal lobe, wernicke’s area, occipital lobe, hypothalamus and pituitary gland (Bohlin, Durwin, & Reese-Weber, 2012). The major lobes of the brain are frontal, occipital, parental and temporal and each of them has different functions during the learning process. Frontal lobe is responsible for higher standard thinking. According to the book, during the learning process, frontal lobe controls attention, creative