Alzheimer’s disease (AD) is characterized as a progressive and irreversible brain disease resulting in the eventual impairment of all cognitive functioning for the affected individual[1]. Despite all current efforts in determining a definite cause for AD, there are three prevailing hypotheses which have been proposed. These involve the oxidative stress, β- amyloid fibril and tau protein hypotheses; all of which are interrelated and are potential mechanisms for the underlying medical condition.
Diagnosis of AD is done with mental-state examinations coupled with functional or structural scans[2]. The combination of tests helps in ruling out other potential mental illnesses that produce similar symptoms. Identification of biomarkers (eg. Tau, β-amyloid[2]) provides a step forward in determining the cause of AD as well as potential therapies that could be used to target the specific biomarkers.
Alzheimer’s disease is known to be correlated with traumatic brain injuries (TBI), as suffering from even one event of TBI has been shown to increase neurofibrillary tangles and amyloid-β plaques[3]. TBI has been shown to up-regulate the enzyme BACE1, which increases amyloid-beta plaques[4]. It also up-regulates apolipoproteins, and possessing a particular allele called apolipoprotein E4 has been correlated with increased susceptibility to developing AD[5].
The current literature regarding the prevention of AD is focused on several avenues of research. The most well researched preventative measures are angiotensin II receptor blockers, vitamin D and omega 3 fatty acids[6]. These 3 mainly target the formation of amyloid plaques and the prevention of oxidative stress on neurons.
Currently there are no methods available for curing AD, but there are a variety of pharmaceutical and psychosocial treatments that can be utilized by patients. There are many on-going experiments and research using alternative methods such as intranasal insulin and methylene blue which have shown great potential in developing a cure.
1.0 Molecular Mechanisms of Pathology: Possible Hypotheses
main article: 1.0 Molecular Mechanisms of Pathology: Possible Hypotheses
author: Joanna Salvatore
| Alzheimer's disease |
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| Image courtesy of ZME Science http://www.zmescience.com/medicine/diseases-medicine/earliest-signs-of-alzheimer-043243/ |
Alzheimer’s disease (AD) is of major concern for the aging population due to its age-dependent onset, and progressive cognitive deterioration of the affected individual[1]. It is known that AD is the primary cause of dementia in the elderly, as well as a leading cause of disability and death[2]. AD is also associated with the significant loss of neurons, and cerebral and hippocampal atrophy[3]. Although the actual process of how the disease begins to arise is not for certain, its development has been suggested to be caused by a succession of events occurring over prolonged periods of time within the brain[1]. Distinct brain lesions further characterize AD, involving neurofibrillary tangles (NFTs), and extracellular plaque formation[4]. The prevailing hypotheses that have been proposed to account for the changes occurring within the brain in AD encompass: oxidative stress, β- amyloid fibril and tau protein hypotheses. These postulations are all interrelated and serve as potential mechanisms for the underlying medical condition.
2.0 Diagnostics of Alzheimer's Disease
main article: 2.0 Diagnostics of Alzheimer's Disease
author: Broencephalon
| PET Scan of the brain: Healthy vs. AD |
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| Image courtesy of the National Institute on Aging/National Institutes of Health |
Alzheimer’s disease (AD) is the most common form of dementia and is a neurodegenerative disease that is most prominent in aged-individuals[1]. Currently, the diagnosis of AD is difficult and comes with a degree of uncertainty. Its diagnosis is difficult because there is no single test that will prove beyond reasonable doubt that an individual has the disease. Similarly, its diagnosis comes with a degree of uncertainty because being the most common form of dementia, it shares many of the common symptoms (e.g. cognitive impairments, brain activity[2]). Tests to determine cognitive function used together in conjunction with modern brain scans and identification of potential biomarkers (e.g. β amyloid and Tau[2-3]) provide physicians with information that is required to generate a reliable diagnosis of AD. The only way to conclusively diagnose AD is to perform a brain biopsy; a clinical diagnosis is done by process of elimination[4] and will contain some degree of uncertainty as previously mentioned.
3.0 Preventing Alzheimer's Disease
main article: 3.0 Preventing Alzheimer's Disease
author: Darren Tan
| Alzheimer's Disease |
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| Courtesy of www.Webicina.com |
Alzheimer's disease (AD) is the only one of the top 10 causes of death in the United States for which concrete strategies of prevention have not been found.[1] By 2050, there are estimated to be 13 million dementia patients in the United States alone.[2] As the most common form of Dementia, it is imperative that possible methods of prevention be found in order to combat this neurodegenerative disease. Several substances have been found to reduce the risk of AD, including Angiotensin II receptor blockers, Vitamin D, and Omega 3 fatty acids. With further research and perhaps application of a combination of these factors, it may be possible to prevent or dramatically reduce the risk of AD.
4.0 Alzheimer's Disease and Traumatic Brain Injury
main article: 4.0 Alzheimer's Disease and Traumatic Brain Injury
author: Karthik Natarajan
| Alzheimer's disease and TBI |
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| TBI is known to have significant correlation with development of Alzheimer's. Image adapted from [4] |
Alzheimer’s disease (AD) is influenced by both genetics and the environment [1]. There has been a significant correlation identified between suffering a traumatic brain injury (TBI) and developing Alzheimer’s disease so TBI is an important environmental factor that can influence development of the disease[2]. TBI is very prevalent in society – each year, 1.7 million people in the United States suffer a head injury[2]. TBI has been shown to cause very similar neurological changes to those observed in Alzheimer’s patients, such as increased neurofibrillary tangles (NFT’s) and amyloid-β plaques which eventually result in neuronal death, through oxidative stress triggering apoptotic cell pathways, and impaired transport and function of mitochondria [2][3].
TBI has been shown to elevate the levels of Aβ producing proteins, thereby increasing Aβ levels. It causes functional changes at the level of the synapse which result in synaptic degeneration. TBI also elevates the levels of proteins involved in Aβ degrading mechanisms, such as neprilysin and apolipoprotein E. However, genetic polymorphisms have been identified in Aβ degrading proteins, which reduce their ability to degrade Aβ. Therefore, formation of long-lasting Aβ plaques following TBI is ultimately dependent on whether or not an individual possesses polymorphisms in Aβ degrading proteins.
5.0 Treatment of Alzheimer's Disease
main article: 5.0 Treatment of Alzheimer's Disease
author: Mingzhe Liu
| Treatment of Alzheimer's Disease |
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| Courtesy of: www.cnn.com |
Alzheimer's disease (AD) is often characterized as both a progressive and irreversible brain disease which has been linked to the eventual loss of all cognitive function [1]. Although AD has been widely studied throughout; at present, there are no methods in which to fully cure AD due to not knowing the underlying cause of the condition. Instead, current methods in treatment aim to alleviate some symptoms of Alzheimer’s disease relying on a variety of pharmaceutical and psychosocial treatments that can be administered to the patient. The 2 main groups of drugs in use are acetylcholinesterase inhibitors and NMDA receptor antagonist, which help to regulate the amount of acetylcholine and glutamine present- allowing for better cognitive functioning [2-3]. As well, it has been shown that psychosocial treatments prescribed in conjunction with pharmaceutical treatments have had great results for patients with AD [4]. Many on-going experiments have also shown great potential in offering a cure, such as Deep Brain Stimulation and Methylene Blue. As with the introduction and development of Magnetic Resonance Image-guided Focused Ultrasound Surgery technology, this has also opened up many new opportunities for the development and incorporation of other treatment methods, such as targeted drug and stem cell delivery to the specific regions of the brain affected by AD.
Your topic seems well-researched and each individual page itself is detailed and provokes interest. You all have very inviting pages as they are immersed with videos and pictures very relevant to each subtopic. It would have been nice to also read any research that may have been done on the stigma of Alzheimer's Disease.