What Is Progressive Age-Related Neururodegenerative Disorder?

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 known to be a neurological disorder of the central nervous system is an irreversible disorder in which brain cells deteriorate resulting to loss of our cognitive functions, primarily memory, movement coordination, reasoning and judgment, and pattern recognition. In its advanced stage, all memory and mental functioning could be lost (Healthcommunities.com, 2016). This disease is known to be caused by parts of the brain shrinking (atrophy), which destroys the structure and function of particular areas of the brain (Nhs.uk, 2016). Although the exact cause to this process is not known, research suggest that in the brains of patients with Alzheimer 's disease, scientists have found amyloid plaques (abnormal deposits of protein), neurofibrillary tangles containing tau and acetylcholine a chemical imbalances (Nhs.uk, 2016).

The present results showed that daily protection with caffeine attenuated the increase in MDA levels in AlCl3-intoxicated rats. Supporting the present finding, previous studies have revealed the antioxidant potential of caffeine against lipid peroxidation in various animal models of neurologic diseases, including Alzheimer’s disease (Prasanthi et al., 2010), epilepsy (Souza et al., 2013) and Parkinson's disease (Khadrawy et al., 2017). It has been demonstrated that caffeine has the ability to scavenge reactive oxygen species (Devasagayam et al., 1996) and modulated the brain antioxidant system through increasing the content of GSH and activities of antioxidant enzymes like glutathione reductase and superoxide dismutase (Abreu et al., 2011). Generally, the antioxidant capacity of caffeine was similar to that of the established biological antioxidant GSH and significantly higher than ascorbic acid (Devasagayam et al., 1996). Accordingly, this may explain the ability of caffeine to attenuate lipid peroxidation induced by AlCl3 in the current study via direct scavenging of reactive oxygen species or by increasing GSH content and antioxidant enzymes activities.

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 inflammation and oxidative stress, so it is important to take the right amount of antioxidant micronutrients like vitamin C and vitamin E as well as anti-inflammatory macronutrients such as omega-3 polyunsaturated fatty acids to protect the brain from ageing (Whalley et. al, 2004). This is a devastating disease that affects most people over the age of fifty. Recently, there have been many studies done to figure out what causes this disease, if there is anything that can cure it, and how to prevent the disease. Seneff, Wainwright, and Mascitelli, believe Alzheimer’s develops with consuming too many carbohydrates, especially fructose and having a deficiency in cholesterol and dietary fats as well (2010). Whalley, Starr, and Deary have seen that poor diet, poverty, and failing health are links to developing Alzheimer’s Disease (2004). Furthermore, seeing increase in plasma homocysteine concentration increases risk of Dementia, which can result from an inadequate intake of vitamin B12/folate (Walley et. al, 2004). Additionally, Gray supports Walley’s findings and even believes having an adequate intake of vitamin B12/folate will have a positive effect on the overall health

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.

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

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

As the leading cause for dementia, Alzheimer’s disease –AD-, effects more than 25 million people in the world (Perrone & Grant, 2015, p. 1).The neurodegenerative disorder, results in behavioral changes, as well as cognitive including, loss of memory and language skills ( Mayo Clinic Staff, 2014). Researchers have tracked two leading abnormalities resulting in Alzheimer’s. These two are, amyloid plaques-clumps of protein which form in and around the neurons- and neurofibrillary tangles- insoluble fibers made up mostly of tau protein- (Mayo Clinic Staff, 2014). Although both are a prevalent indication of AD, scientist have not been able to indicate whether these are merely a byproduct or a cause. Hence, call for epidemiological research is ongoing. Earlier studies have suggested a link between diabetes- specifically, Type 2 diabetes mellitus- and AD (Paddock, 2015). These observations suggest the metabolic processing of glucose is abnormal, and this plays a role in AD pathogenesis (Macauley et al., 2015).Recently, studies have linked, a dietary relevance of advanced glycogen end products, or AGEs, to the incidence of AD (Perrone & Grant, 2015, p. 2). AGEs are also called glycotoxins, because they increase the risk of diseases such as diabetes, cardiovascular disease, and several other aging related-diseases, such as AD (Perrone & Grant, 2015, p. 2). More on, as with diabetes and AGEs , researchers have directly linked high blood sugar to the production of beta-amyloid, in

“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

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

Known as the fifth leading cause of death in the United States, Alzheimer’s disease (AD) affects approximately 5.3 million Americans and is the major cause of dementia. Although the cause of AD is unknown, the correlation between the damage caused by plaque in the brain and evidence of the disease suggests possible causality. Indicated by extracellular dense plaques and intracellular neurofibrillary tangles made of beta-amyloid and tau proteins, respectively, this neurodegenerative disease is thought to be a result of mutations in the amyloid precursor protein (APP), the genetic precursor of beta-amyloid peptides.

Another important consequence of heightened levels of Aβ 42 is the disruption of astrocytes responsible for regulating Ca2+ levels in the extracellular space of neurons which is essential for Ca2+ cascades. When Aβ 42 oligomers are released from neurons, they can bind to receptors on partner astrocytes and cause the astrocytes to release glutamate which is then taken up by NMDA receptors. The resultant signal cascade causes surges in Ca2+ evoking a cascade of events, including oxidative damage from dysfunctional mitochondria, tau hyperphosphorylation, the destruction of dendritic spines and neuronal synapses, and severing communications within the astrocyte’s neurons and beyond (Kumar et al., 2015).

There have been a few alternative theories proposed to explain what directly causes Alzheimer’s. One called the Inverse Warburg effect focuses on age-induced energy deficiency seen in mitochondrial activity of neurons (Demetrius et al. 2015). Energy, produce mainly by mitochondria, is

Oligodendrocytes are the most vulnerable brain cells to oxidative stress due to its high metabolic demand for synthesizing myelin sheaths (Ichinose et al., 2014), and relatively low levels of antioxidants (Lassmann and Van Horssen, 2011). Accumulating evidence suggests that oxidative stress plays a major role in the pathogenesis of MS. In the present study, cuprizone diet significantly increased brain TBARS level and decreased GSH content. These results are consistent with previous reports which reported that reactive oxygen species (ROS), produced as a consequence of alteration in the mitochondrial electron transport chain, have been implicated as mediators of demyelination and axonal damage in both MS and its animal models (Ghaiad et al., 2017; Kashani et al., 2014). On the other hand, treatment with linagliptin showed significant reduction in TBARS level and increase in GSH