Aggression in Brain Injury, Aging, and Neurodegenerative Disorders

2003 ◽  
pp. 151-165
Author(s):  
Mark P. Mattson
2009 ◽  
Vol 108 (6) ◽  
pp. 1343-1359 ◽  
Author(s):  
Nicholas P. Whitney ◽  
Tess M. Eidem ◽  
Hui Peng ◽  
Yunlong Huang ◽  
Jialin C. Zheng

2010 ◽  
Vol 31 (5) ◽  
pp. 852-863 ◽  
Author(s):  
Charlotte Israelsson ◽  
Henrik Bengtsson ◽  
Anna Lobell ◽  
Lars N. G. Nilsson ◽  
Annika Kylberg ◽  
...  

2016 ◽  
Vol 1 (1) ◽  
pp. 57
Author(s):  
Raunak Varshney ◽  
Anil K. Mishra

<p>A silent epidemic of modern world and largely neglected field in drug development is traumatic brain injury. There is no treatment available for the patients suffering from brain trauma. Peptide is a naturally occurring biological alternative that could represent a new generation of future medications. In this study, we have designed and modified the C-terminal amino acids of KDI peptide responsible for neurite growth. The inclusion of a Cys (C), Gly (G), Cys and Pro (P) amino acids in the sequence leads to the possibility of better binding with the target receptor 3T1M as compared to the known KDI sequence for neurite growth. Studies on human SH-SY5Y cells for neurite outgrowth demonstrates that the CGCKDP could plausibly be useful in neuroregeneration in neurodegenerative disorders by neurite growth formation.</p>


2016 ◽  
Vol 27 (1) ◽  
pp. 93-100 ◽  
Author(s):  
Rajaneesh Gupta ◽  
Nilkantha Sen

AbstractTraumatic brain injury (TBI), a major global health and socioeconomic problem, is now established as a chronic disease process with a broad spectrum of pathophysiological symptoms followed by long-term disabilities. It triggers multiple and multidirectional biochemical events that lead to neurodegeneration and cognitive impairment. Recent studies have presented strong evidence that patients with TBI history have a tendency to develop proteinopathy, which is the pathophysiological feature of neurodegenerative disorders such as Alzheimer disease (AD), chronic traumatic encephalopathy (CTE), and amyotrophic lateral sclerosis (ALS). This review mainly focuses on mechanisms related to AD, CTE, and ALS that are induced after TBI and their relevance to the advancement of these neurodegenerative diseases. This review encompasses acute effects and chronic neurodegenerative consequences after TBI for a better understanding of TBI-induced neuronal death and to design therapies that will effectively treat patients in the primary or secondary progressive stages.


Author(s):  
Walter Glannon

Arguments for moral and criminal responsibility generally assume that the control necessary for responsibility rules out all forms of brain manipulation. The agent’s mental states must be the direct causes of her actions. Yet when they operate effectively, neuroprosthetics do not undermine but restore control of motor and mental functions that have been lost from brain injury or impaired by neurodevelopmental and neurodegenerative disorders. Neural implants enable varying degree of voluntary agency by restoring varying degrees of the relevant functions. Whether or to what extent a person with a device implanted in her brain can be criminally responsible for an action, omission or consequence of an action or omission depends on the extent to which she can control the device and the thought and behavior it is designed to regulate. I present actual and hypothetical cases involving three different types of brain implants to explore how individuals with these devices implanted in their brains can control their mental states and actions. Brain implants that alter motor and mental functions should make us reconsider standard interpretations of psychological and physical criteria of criminal responsibility.


2021 ◽  
pp. 131-155
Author(s):  
Eliyas Jeffay ◽  
Kyrsten M. Grimes ◽  
Konstantine K. Zakzanis

Traumatic brain injury (TBI) is a craniocerebral trauma associated with decreased level of consciousness, amnesia, and potential abnormalities on neuroimaging. Apathy is a common symptom after TBI with a wide prevalence range (11–71%), which may be due to assessment, overlapping symptoms with depression, time since injury, and severity of injury. There is a dearth of studies exploring the neurobiology of apathy after TBI but patterns indicate the involvement of the prefrontal cortex, anterior cingulate cortex, and insula. These areas are also commonly disrupted after a TBI. Little is known regarding the neuropsychology of apathy and TBI with some evidence of executive dysfunction and acquisition memory deficits. Similarly, there is limited evidence for treatment of apathy after TBI. Many interventions implemented to date were based on empirically based interventions for neurodegenerative disorders. This review is intended to raise clinicians’ awareness of apathy after TBI and encourage researchers to explore this emerging phenomenon.


2016 ◽  
Vol 69 ◽  
pp. 381-401 ◽  
Author(s):  
Claire Kos ◽  
Marie-José van Tol ◽  
Jan-Bernard C. Marsman ◽  
Henderikus Knegtering ◽  
André Aleman

2017 ◽  
Vol 12 (1) ◽  
Author(s):  
Merry W. Ma ◽  
Jing Wang ◽  
Quanguang Zhang ◽  
Ruimin Wang ◽  
Krishnan M. Dhandapani ◽  
...  

2019 ◽  
Vol 42 ◽  
Author(s):  
Colleen M. Kelley ◽  
Larry L. Jacoby

Abstract Cognitive control constrains retrieval processing and so restricts what comes to mind as input to the attribution system. We review evidence that older adults, patients with Alzheimer's disease, and people with traumatic brain injury exert less cognitive control during retrieval, and so are susceptible to memory misattributions in the form of dramatic levels of false remembering.


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