Alzheimer's Disease, Neuropsychology of

Morris, Robin G.; Worsley, Claire L.

doi:10.1016/b0-12-227210-2/00020-0

Cited by 2 publications

(1 citation statement)

References 4 publications

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“…The TBI mice display AD‐like learning and memory impairments, AD‐like tau phosphorylation at several sites and loss of synapses one month after TBI, which is consistent with previous studies 7,34 . These data support an opinion that TBI and AD share similar pathological features such as the presence of abnormal tau phosphorylation (main component of neurofibrillary tangles), loss of synapse and cognitive deficits 45 . As we known, there are currently no efficient drugs for AD.…”

Section: Discussionsupporting

confidence: 90%

The overexpression of RBM3 alleviates TBI‐induced behaviour impairment and AD‐like tauopathy in mice

Liu

Cao

Shi

et al. 2020

J Cellular Molecular Medi

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Alzheimer disease (AD) is the most common form of dementia in older individuals and probably develops as a result of complex interactions among multiple factors, including age, genetics, environment, lifestyle and traumatic brain injury (TBI). 1-5 The evidence has shown that there appears to be a strong link between future risk of Alzheimer's and serious TBI, but how TBI increase future risk of AD is still unclear. 6-8 TBI caused by contact sports, work accident or military blasts may induce acute or potentially long-lasting neurological dysfunction, including chronic traumatic encephalopathy. 4-6,8,9 The clinical features of TBI vary depending on the mechanistic types and severity of head injury. These features generally consist of cognitive

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Section: Discussionsupporting

confidence: 90%

The overexpression of RBM3 alleviates TBI‐induced behaviour impairment and AD‐like tauopathy in mice

Liu

Cao

Shi

et al. 2020

J Cellular Molecular Medi

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Evaluating action possibilities: a procedural metacognitive view of intentional omissions

Kärki

2024

Philos Stud

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How do we control what we do not do? What are the relevant guiding mental states when an agent intentionally omits to perform an action? I argue that what happens when an agent intentionally omits is a two-part metacognitive process in which a representation of an action is brought to the agent’s mind for further processing and evaluated by her as something not to be done. Without a representation of the action not done, the agent cannot further process the possibility of her own action; she cannot intentionally try to not do something, resist performing an action, or decide or choose to not perform an action. The literature on people with frontal lobe damage suggests that without metacognitive control of action, a person automatically follows what the environment affords or what others are doing. Through at least procedural metacognitive control of action, agents are able to intentionally omit. This view has explanatory power over a variety of intentional omissions and over a variety of agents. It answers central questions in the philosophy of intentional omissions: who is capable of intentionally omitting, when and where intentional omissions unfold, and what are the relevant guiding mental states on which the control of intentional omissions is based? The answers to these questions contribute in part to naturalizing agency, at least when it comes to negative agency, our ability to guide the non-performance of our actions.

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Alzheimer's Disease, Neuropsychology of

Cited by 2 publications

References 4 publications

The overexpression of RBM3 alleviates TBI‐induced behaviour impairment and AD‐like tauopathy in mice

The overexpression of RBM3 alleviates TBI‐induced behaviour impairment and AD‐like tauopathy in mice

Evaluating action possibilities: a procedural metacognitive view of intentional omissions

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