Publications by authors named "Desarae A. Dempsey"

Article Synopsis
  • Traumatic brain injury (TBI) may be linked to an increased risk of Alzheimer's disease (AD), potentially due to its influence on the onset of cognitive symptoms and pathological protein deposition, although the exact mechanisms remain unclear.
  • A review of studies utilizing PET imaging to measure β-amyloid and tau in individuals with a history of TBI highlighted common methodological issues and found inconsistent results, particularly concerning sample size and reliance on self-reported TBI.
  • The most compelling evidence for increased β-amyloid was found in the cingulate gyrus and cuneus/precuneus, while tau showed elevated levels in various brain regions, though conflicting results underscore the need for further research with larger, more detailed studies.
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Article Synopsis
  • Limited research has examined how cardiovascular risk and amyloid levels influence cognitive decline in East Asians, specifically in a study involving 526 participants from the Korean Brain Aging Study.
  • Results showed that cognitively normal individuals without amyloid (Aβ-) but with high cardiovascular risk scores had significantly lower cognitive performance than their low-risk counterparts.
  • Ultimately, while managing vascular risk is important for early cognitive preservation in Aβ- individuals, amyloid pathology was found to be the main factor driving cognitive decline in both cognitively normal and mild cognitive impairment groups, regardless of vascular risk status.
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The BrainAGE method is used to estimate biological brain age using structural neuroimaging. However, the stability of the model across different scan parameters and races/ethnicities has not been thoroughly investigated. Estimated brain age was compared within- and across- MRI field strength and across voxel sizes.

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Traumatic brain injury (TBI) has been discussed as a risk factor for Alzheimer's disease (AD) due to its association with dementia risk and earlier cognitive symptom onset. However, the mechanisms behind this relationship are unclear. Some studies have suggested TBI may increase pathological protein deposition in an AD-like pattern; others have failed to find such associations.

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Like many social behaviors, aggression can be rewarding, leading to behavioral plasticity. One outcome of reward-induced aggression is the long-term increase in the speed in which future aggression-based encounters is initiated. This form of aggression impacts dendritic structure and excitatory synaptic neurotransmission in the nucleus accumbens, a brain region well known to regulate motivated behaviors.

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