آسیب های مغزی: یک عامل خطرساز برای بیماری آلزایمر
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|30772||2012||6 صفحه PDF||سفارش دهید||7536 کلمه|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Neuroscience & Biobehavioral Reviews, Volume 36, Issue 5, May 2012, Pages 1376–1381
Traumatic brain injury (TBI) constitutes a major global health and socio-economic problem with neurobehavioral sequelae contributing to long-term disability. It causes brain swelling, axonal injury and hypoxia, disrupts blood brain barrier function and increases inflammatory responses, oxidative stress, neurodegeneration and leads to cognitive impairment. Epidemiological studies show that 30% of patients, who die of TBI, have Aβ plaques which are pathological features of Alzheimer's disease (AD). Thus TBI acts as an important epigenetic risk factor for AD. This review focuses on AD related genes which are expressed during TBI and its relevance to progression of the disease. Such understanding will help to diagnose the risk of TBI patients to develop AD and design therapeutic interventions.
National Head Injury Foundation (1988) has defined traumatic brain injury (TBI) as “an insult to the brain caused by an external force that may produce diminished or altered states of consciousness, which results in impaired cognitive abilities or physical functioning”. About 1.4 million people suffer from TBI every year in the United States alone (Zohar et al., 2011). The yearly cost of acute care and rehabilitation for new cases in the United States is between $9 and $10 billion (NIH Consensus Development Panel, 1999). TBI affects all age groups with particular prevalence among children and young adults (Fins, 2003 and Kövesdi et al., 2010). It is the leading cause of acquired disability in children (Cronin, 2001). Survivors of TBI suffer from a wide variety of pathologies such as neurological deficits, short and long term brain damage, cognitive, behavioral and emotional impairments, all of which depend on the severity of injury. Neurological deficits in cognition are due to atrophy of hippocampus and damage of white matter tract as evident from functional imaging studies (Atkins et al., 2009). TBI can be classified as (i) focal damage, which occurs in localized area and causes damage to the underlying brain tissues and vessels, and (ii) diffuse damage, which is not restricted but widespread throughout the brain. Diffuse type mainly involves axonal injury also called diffuse axonal injury (DAI), brain swelling and hypoxia (Hellewell et al., 2010 and Laurer et al., 2000). Axonal injury is an almost universal sequel of TBI (Li et al., 2006 and Smith, 2000) and a powerful predictor of morbidity and mortality (Czeiter et al., 2008). In axons, it causes an accumulation of proteins, including amyloid precursor protein (APP), which is carried by fast anterograde axonal transport and serves as a sensitive marker of axonal damage. This may result in axonal disconnection leading to loss of axonal function and structure (Chen et al., 2004). TBI is one of the most consistent candidates for initiating the molecular cascades that result in Alzheimer's disease (AD), Parkinson's disease (PD) and amyotrophic lateral sclerosis (Gavett et al., 2010).