Alzheimer's Main Features

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

1.1 Dementia is an umbrella term for a range of diseases that affect memory, behaviour and motor skills. The causes vary depending on the disease but largely the presence of “plaques” and “tangles” on the neurons of the brain is found in people with Alzheimer’s. Plaques are protein that the body no longer breaks down and allows to build up; these get between the neurons and disrupt the message transmission. Tangles destroy a vital cell transport system made of proteins. The transport system is organised in orderly parallel strands like rail tracks. In healthy areas a protein call “tau” helps the tracks stay straight but in areas where tangles

Alzheimer's disease is one of the most common causes of dementia. The term 'dementia' describes a set of symptoms, which can include memory loss, changes in mood and problems with communication and reasoning. These symptoms occur when certain diseases and conditions, including Alzheimer’s disease, damage the brain. Alzheimer's disease could be described as a physical disease affecting the brain. During the course of the disease, protein 'plaques' and 'tangles' develop

Alzheimer’s: Scientists know that during Alzheimer’s two abnormal proteins build in the brain. They form clumps called either ‘plaques’ or ‘tangles’. These plaques and tangles interfere with how brain cells work and communicate with each other. The plaques are usually first seen in the area of the brain that makes new memories. A lot of research is focused on finding ways to stop these proteins in their tracks and protect brain cells from harm.

Alzheimer‘s disease disrupts the regular functioning of the brain, bringing about dementia (Patterson et al., 2008). A patient’s mental clarity, memory, and sometimes language abilities progressively decline with time. The disease brings about physical changes inside the brain, whereby certain regions of brain matter enlarge while others shrink. When brain parts enlarge or shrink, the normal links inside get broken, interrupting

The causes of Alzheimer’s are not yet fully understood; however, its effect on the brain can be understood. Alzheimer’s disease - insidious, attacking and terrifying - stalks and then murders brain cells. A brain afflicted with Alzheimer’s disease has a decreased count in cells and connections among cells. The more brain cells die, the smaller the brain of a person with Alzheimer’s gets. When doctors examine a brain with Alzheimer’s tissue, they see two types of deformities that are known to be trademarks of the disease. The first trademark is known as plaque, which is a cluster of a beta-amyloid protein that may damage and kill brain cells in a number of ways, including blocking with cell-to-cell communication. Whereas the final cause of brain-cell death in Alzheimer’s remains a mystery, the groups of beta-amyloids that cover the brain cells are a sure sign of the disease. The second trademark of Alzheimer’s is the tangle. Brain cells are reliant on internal support and a transport system to bring nutrients and other essentials to their distant regions. This system needs a protein called tau. In Alzheimer’s, strings of tau protein roll into abnormal tangles inside brain cells, concluding in failure of the cell's transport system. This breakdown of the system is powerfully involved in the decline and death of brain

Alzheimer's disease is characterized by the formation of amyloid plaques and neurofibrillary tangles in the cortex, entorhinal cortex and hippocampus of the brain causing neuronal cell death, dysfunction of neurotransmitters (acetylcholine, serotonin, and norepinephrine) and atrophy in affected areas. B Amyloid plaques are described as insoluble clumps of peptides resulting from the cleavage of amyloid precursor protein. Neurofibrillary tangles result from destruction of neuronal microtubules which are key components of neuronal cell structure as they deliver nutrients and assist with synaptic

“Alzheimer’s Disease (AD) is a type of dementia, which is affecting the population that develops in the brain and can lead to problems with memory, thinking and behavior”. The Amyloid Hypothesis claims that the build up of the beta-amyloid in the brain is a cause in the development of Alzheimer disease in patients. This plaque of the beta-amyloid and its cascade of events can be linked to the deterioration and negative effects of cognitive function of the brain over time. The beta-amyloid is described to be a “sticky” protein located in the brain therefore plaques or build up of the amyloid is common. These plaques in turn can block the brain cells from communicating with each other. Which then activates an immune system, that leads to inflammation

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

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

Alzheimer's disease is a progressive degenerative disease that affects the brain. It causes mental deterioration in the brain and may occur in middle or old age. Ultimately, a person with AD loses all memory and mental functioning over time. The disease slowly destroys memory and thinking skills, and eventually the ability to do simple tasks. Alzheimer’s is named after Dr. Alois Alzheimer, who noticed changes in the brain tissue of a women who had died of an unusual mental illness. She showed symptoms like memory loss, language problems and unpredictable behavior. He examined her body and found abnormal clumps (now diagnoses as amyloid plaques). These clumps are now considered one of the main features of alzheimer's

The research into Alzheimer's Disease has come a long way since 1906 when it is was discovered by Alois Alzheimer. He detected microscopic brain tissue changes called senile and neuritic plaques in deceased patients. These are chemical deposits consisting of protein molecules called Amyloid Precursor Protein(APP) that are fundamental components of a normal brain. However in the brain of an Alzheimer patient, an enzyme cuts the APP apart and leaves fragments in the brain tissue. These combined with degenerating nerve cells cause the plaques or lesions. These lesions are found in many sections of the brain including the hippocampus which regulates emotion and memory, the basal forebrain, and especially the basal nucleus of Meynert and the cortex, where the memory function is located.(2) Another sign of a diseased brain are neurofibrillary tangles, which are malformations within nerve cells.

Individuals with Alzheimer’s disease show two types of abnormal lesions that clog their brain: Beta-amyloid plaques—sticky clumps of protein fragments and cellular material that form outside and around neurons; and neurofibrillary tangles—insoluble twisted fibers composed largely of the protein tau that build up inside nerve cells. However scientists are unclear whether these lesions actually cause the disease or if they are just a byproduct of the disease. (Mayo Clinic, 2014) Some early signs and symptoms of Alzheimer’s Disease include memory loss that interrupts daily life, confusion with time or place, trouble understanding visual images and spatial relationships, new problems with speaking or writing, withdrawal from work or social activities, and changes in mood and personality.

Alzheimer’s disease looks to be caused by an accumulation of neurotoxic proteins in the cerebrum, this is the part of the

Since the protein does not disintegrate, it amasses into neuritic plaques (The Alzheimer's Project, 2009). The neurofibrillary tangles structure inside neurons and are made out of matched helical fibers, neuropil strings and dystrophic neuritis. Nfts cause the breakdown of the vehicle framework, as tau protein tumbles off and starts to cluster together, framing tangles, irritating the correspondence between neurons, prompting neuronal demise showed through dementia. The neuropathological criteria for an AD analysis are focused around the recurrence of the decrepit plaques and the geography of the neurofibrillary tangles (Goetz, 2007). The cerebrocortical decay prompts the decrease of the mind with twenty percent or more. The