This literature review is an investigation of traumatic brain injury and Alzheimer’s disease in various experimental methods. Participants were taken from a range of demographic areas and were either observed or experimented upon. Blunt force trauma to the cranium is shown to be an association with late-onset Alzheimer’s disease in animal models and human observation.
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The results in all studies are shown to be consistent with the previously accepted notion of traumatic brain injury being extremely correlated to the contraction of Alzheimer’s disease. Methodology included experimentation on mouse models, inducing traumatic brain injury, and the observation of traumatic brain injury in practical environments. Further research is needed to draw a baseline correlation between traumatic brain injury and Alzheimer’s disease.
The Correlation of Traumatic Brain Injury and Alzheimer’s Disease: A Literature Review Research on neurodegenerative diseases has taken a notable approach to discovering their underlying causes and correlations. Alzheimer’s Disease (AD) has been the leading cause of dementia for over a century (Nogueira et al., 2016). There are discrepancies between research and diagnosis; very few cases of AD have a definitive cause. Traumatic brain injury (TBI) has been linked to AD in many circumstances. From spontaneous accidents causing blunt trauma to the head, battleground combat in our military, to the widely accepted sports like American football and professional fighting; cases of TBI are increasing exponentially and interestingly enough, the same trend applies to AD. Researches are continuously searching for answers and ways to circumvent or mitigate the effects of TBI, which could lower the rate of contraction of AD in our society.
AD is a form of dementia; it is a neurodegenerative disease that affects the natural cognitive functions of a normal functioning brain. Alzheimer’s has a couple main signs that characterize the pathology of the disease. This form of dementia intrinsically affects cholinergic neuronal cell lines by a rogue protease that incorrectly cuts a protein, called the amyloid precursor protein (APP), causing amyloid-beta deposits or plaques to build up in the extracellular matrix of a neuronal cell (Kondo et al., 2015). The second sign of AD is from the hyper phosphorylation of tau protein that is responsible for microtubule formation. The hyper phosphorylation induces an event called catastrophe, which is the sudden degradation of microtubule formation causing neurofibullary tangles to accumulate in the intracellular matrix of a neuronal cell. Both of these processes cause defects in cell communication and neuronal
Plasticity, ultimately causing the prevailing symptoms of memory loss, language impairment and reasoning deficits. A plethora of suggestions are made depicting the origin of AD, but a sole cause is not defined.
Severe trauma anywhere to the human body will pose detrimental effects and can be treated naturally or by modern medicine, but an injury that shows no definitive treatment options is traumatic brain injury (TBI). Our brain defines our character and uniqueness; severe trauma to this body organ can lead to irreversible damage affecting cognitive ability. Consequences of TBI can lead to impairments in memory, reasoning, and motor skills (O’Connor et al., 2013). Symptoms present themselves in various ways; there may be immediate signs of ailments and debilitations, or manifestations could prolong to appear for weeks or even months post trauma. Current research has discussed the relationship of TBI with various neurodegenerative diseases. Further research is needed to establish connections between brain trauma and cognitive diseases. Hypothesis
If the recognition and dissemination of more research on the correlation of AD and TBI are conducted, then policies can be put in place to mitigate the contraction of AD.
Participants used in all studies had shown signs of TBI, signs of AD, or were patients of late-onset AD due to unexplainable corollaries. Empirical studies were conducted on model organisms to assess the consequences of TBI along a time span by biochemically analyzing their neuronal development. All human studies required participants to have a documented case of TBI or AD with telltale signs of amyloid-beta plaques and fibrils.
Physical stress and TBI. Medical professionals and researchers are well aware of how TBI occurs: blunt force trauma to the head is caused by injury, physical attack, or forceful impact to the cranium (Gileen, Greenwood, & David, 2013). In all research reviewed, physical stress and TBI were analyzed by various experimentation to determine its’ holistic effects. Physical stress and trauma were either mechanically induced to a model organism or observed within many of participants. All studies observed show features of amyloid-beta and tau protein accumulation alongside dysfunction in neuronal-cell plasticity in relation to TBI and physical stress (Nogueira, Epelbaum, Steyaert, Dubois, & Schwartz, 2016). These studies inform researches about the harmful effects of TBI and its’ severity. Continued research would aid in making connections with blunt-force trauma and deficits in our working memory.
Assessment of working memory. In all studies conducted, the comprehensive objective was to assess the effects of TBI analyze relationships to working memory. The hippocampus plays a critical roll in memory acquisition and consolidation; trauma to these regions could manifest into deficits in function including memory and lack of awareness (Gilleen, Greenwood, & David, 2013; O’Connor et al., 2013). The austerity of the effects TBI elicits can vary across patients, but the more severe injuries transcend enduring damage (O’Connor et al., 2013). These findings help show the interconnection between TBI and hippocampal dysfunction, creating a possible parallel between brain trauma and neurodegenerative disorders.
TBI elicits signs of AD. Since the widely accepted signs of AD are so prevalent, studies have been done to observe the correlations between TBI and the accepted signs of AD. In the studies reviewed, results suggest that exposure to cranial traumatic stress is associated with decreased memory performance and motor deficits (Shishido et al., 2016;Weiner et al., 2017; & Gileen et al., 2013). Injury to the brain affects learning and memory acquisition at an escalated rate as age increases (O’Connor et al., 2013). Although there are no studies that show a definitive causal relationship between TBI and AD, the results show a significant correlation. Shishido et al. (2016) found that mice exposed to TBI show an increased concentration of amyloid-beta plaques and tau fibrils in their cholinergic neurons. Further empirical studies depicting the relationship between TBI and AD are imperative to finding ways to prevent forms of dementia.
Type of study. Studies conducted show differences in experimental design, types of participants, and the level of study. Although all studies showed empirical experimentation, various studies relied on manipulating animal models in the lab while others performed quasi- like experiments on military veterans and extreme sport athletes. For example, one study investigated the effects of TBI in snowboarders between increased or decreased use of a helmet, while another study observed the effects of TBI in rat models (Hasler, Baschera, Taugwalder, Exadaktylos, & Raabe, 2015; Nogueira, Epelbaum, Steyaert, Dubois, & Schwartz, 2016). The model organisms used in these experiments help us translate our findings into tangible evidence that could be used for preventive measures.
The model organism used. Results are interpreted differently depending on what type of model organism was utilized in the study. External validity holds an experiment accountable for replication in the real world; observations of TBI and AD vary in contingency whether an animal model or a human model is assessed. In several studies, a mouse model was used to assess consequences of TBI and their correlations to the signs of AD (Shishido et al., 2016). Current research is being conducted to show the associations of various cranial traumas to TBI and other diseases.
Associations with brain injury. Many forms of neurodegenerative diseases could be linked to TBI the studies that were observed differed in the form of brain trauma. For example, war veterans that were affected by TBI were used in a study to make connections to AD, while a study on snowboarders and their helmet use showed compelling evidence of TBI and associations with brain trauma (Hasler, Baschera, Taugwalder, Exadaktylos, & Raabe, 2015; Weiner et al., 2017). Studies on the associations of TBI and various cognitive diseases are essential to combating the attainment of dementia and dangerous ailments.
On-going research has suggested that traumatic brain injuries, which occur in various ways, lead to the progression of AD. Dementia is simply termed to be a decline in cognitive ability severe enough to significantly reduce an organism’s ability to perform everyday activities. AD, the most common form of dementia, is a neurodegenerative disorder associated with synaptic loss, functional abnormalities within neurons, neuronal cell death, an extracellular accumulation of amyloid-B peptide (AB) plaques/fibrils, and an intracellular accumulation of
Hyper phosphorylated tau protein (Iqbal and Grundke-Iqbal, 2013). Accumulation of AB plaques and tau protein fibrils are what cause the gradual decrease in cognitive ability and possible cell death in association with AD (Texido et al., 2012). We hypothesize that if the recognition and dissemination of more research on the correlation of AD and TBI are conducted, then policies can be put in place to mitigate the contraction of AD.
Studies suggest that TBI is becoming an epidemic and a public health initiative that needs to be addressed. Shishido et al. (2016) showed that TBI activates progressive accumulation of amyloid-beta plaques to the injured cortex within one-day post injury. Moderate to severe cases of TBI are correlated with an elevated risk of dementia (O’Connor et al., 2013). Emotional consequence, behavioral impulsivity and aggression are secondary effects of TBI that lead researchers to believe there is a strong association with dementia and hippocampal abnormalities. Alterations in cognitive ability due to TBI include deficits in attention, processing speed, and executive functioning (O’Connor et al., 2013). Physical consequences of TBI can include problems in balance, fatigue, seizures and headaches. Medical consequences of TBI raise concerns that need to be addressed, even without the association of AD or other dementias.
TBI is only one suggested correlation to AD, there are a myriad of associations that could be attributable to the etiology. Gilleen, Greenwood, & David, (2014) suggested that genetic predispositions are a plausible cause for AD. The epidemiology is associated with deficits to the hippocampal regions in the brain, which are responsible for memory consolidation and retrieval. Chronic traumatic encephalopathy (CTE) is correlated with AD and TBI in post mortem neuronal tissues (O’Connor et al., 2013). Athletes experience an increased contraction of CTE while diagnosed with a severe concussion or TBI, which increases symptoms that could cause lifelong
Impairment. Although there is no clinical diagnosis of CTE presently, the disease appears to show extreme pathological correlations with AD and is a consequence of TBI (O’Connor et al., 2013).
It is necessary to continue empirical research on both animal models and humans to document a baseline for treatment and prevention. Limitations of the studies observed include discrepancies in observation and experimentation, which affect the external validity of the study. It is difficult to diagnose a TBI, especially when cases of dementia appear to have similar signs. It is not known whether a TBI-related dementia exists, but further research is needed to establish a template for diagnosis and circumvention.
Inclinations of AD suggest a multitude of causes and relationships. A suggestion for further study could be a longitudinal study to assess a cohort of participants for a set amount of years that experience TBI and those who are genetically predisposed to AD. Genetic predispositions account for a large portion of dementias, but it is imperative to understand the environmental effects that could be attended through practice and prevention by experimentation. Current funding for Alzheimer’s disease does not equate to the exponential rising in rates for diagnosed patients. Despite these growing rates, recent classes of Congress, specially the 112th, have voted no on allowing additional funding to be allocated to the research for and prevention of Alzheimer’s disease. It will be critical to society to diminish the ignorance of relevance that Alzheimer’s disease has and truly takes place. Allowing and funding institutions such as the National Institute of Health to conduct further research on the topic is imperative to put a slash in
The exponential growth that it has taken. Alzheimer’s effects many, but many do not recognize the pain that it causes until it has caused themselves pain.
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