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Posts Tagged ‘middle-age’

Alzheimer plaques in brain injury

Larry H. Bernstein, MD, FCAP, Curator

LPBI

 

Alzheimer’s Plaques Linked to Brain Injury in Middle-Aged People

Bevin Fletcher, Associate Editor   http://www.biosciencetechnology.com/news/2016/02/alzheimers-plaques-linked-brain-injury-middle-aged-people

(Image: Shutterstock)

http://www.biosciencetechnology.com/sites/biosciencetechnology.com/files/shutterstock_111506315.jpg

A new Neurology study, building on other evidence linking head injury to dementia, has found people with brain injuries may have buildup of plaques related to Alzheimer’s disease.

A team, including lead author Dr. Gregory Scott, of Imperial College London in the United Kingdom, performed PET and MRI brain scans on nine people with a single moderate to severe traumatic brain injury (TBI).  Participants had an average age of 44 and suffered their brain injury between 11 months and up to 17 years before the study began.   The brain scans of people with TBI were compared to brains of nine healthy participants and 10 people with Alzheimer’s disease.

The findings were published Wednesday, February 3.

They found that head trauma can sometimes cause the buildup of plaques associated with Alzheimer’s.

“Whilst other studies have shown this, and some very directly through autopsy, ours is the first to look at TBI patients this late on after their injury, and to relate the findings to white matter damage,” Scott told Bioscience Technology.

The researchers found patients with more damage to the brain’s white matter had an increase in plaques.  Both people with Alzheimer’s disease and those with TBI had plaques in the posterior cingulate cortex, an area affected in the beginnings of Alzheimer’s.  Plaques were found in the cerebellum only in participants with TBI. Healthy participants had relatively little or no plaque buildup compared to the other two groups.

“It suggests that plaques are triggered by a different mechanism after a traumatic brain injury,” study author Professor David Sharp, M.D., also of Imperial College London, said in a prepared statement. “The damage to the brain’s white matter at the time of the injury may act as a trigger for plaque production.

If larger studies confirm the findings, then it may help neurologists to target treatments to fend off the disease earlier, Sharp added.

“The areas of the brain affected by plaques overlapped those areas affected in Alzheimer’s disease, but other areas were involved,” Sharp said. “People after a head injury are more likely to develop dementia, but it isn’t clear why.  Our findings suggest TBI leads to the development of the plaques which are a well-known feature of Alzheimer’s disease.”

Up next, Scott told Bioscience Technology, the team is studying inflammation in the brain after TBI and how it relates to brain injury and whether it can be treated.

 

Amyloid pathology and axonal injury after brain trauma

Gregory ScottAnil F. RamlackhansinghPaul EdisonPeter HellyerJames Cole,…., David J. Sharp

http://www.neurology.org/content/early/2016/02/03/WNL.0000000000002413

Objective: To image β-amyloid (Aβ) plaque burden in long-term survivors of traumatic brain injury (TBI), test whether traumatic axonal injury and Aβ are correlated, and compare the spatial distribution of Aβ to Alzheimer disease (AD).

Methods: Patients 11 months to 17 years after moderate–severe TBI underwent 11C-Pittsburgh compound B (11C-PiB)-PET, structural and diffusion MRI, and neuropsychological examination. Healthy aged controls and patients with AD underwent PET and structural MRI. Binding potential (BPND) images of 11C-PiB, which index Aβ plaque density, were computed using an automatic reference region extraction procedure. Voxelwise and regional differences in BPND were assessed. In TBI, a measure of white matter integrity, fractional anisotropy, was estimated and correlated with 11C-PiB BPND.

Results: Twenty-eight participants (9 with TBI, 9 controls, 10 with AD) were assessed. Increased 11C-PiB BPND was found in TBI vs controls in the posterior cingulate cortex and cerebellum. Binding in the posterior cingulate cortex increased with decreasing fractional anisotropy of associated white matter tracts and increased with time since injury. Compared to AD, binding after TBI was lower in neocortical regions but increased in the cerebellum.

Conclusions: Increased Aβ burden was observed in TBI. The distribution overlaps with, but is distinct from, that of AD. This suggests a mechanistic link between TBI and the development of neuropathologic features of dementia, which may relate to axonal damage produced by the injury.

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