Trans-incarceration: Reimagining confinement and the criminality of aging.

As the U.S. population continues to age and will require increasing levels of care, scholars continue to question what conventional methods of "custodial care" and rehabilitation accomplish for the individuals receiving them, relative to those providing them. To this end, critical discourse surrounding the spatial institutionalization of older adults argues that formal institutions of care and rehabilitation are simply alternative and synonymous forms of incarceration and imprisonment. Using semi-structured interviews with ten male residents of a Rhode Island nursing home and ten incarcerated males at the Rhode Island state prison's medium security unit, this work explores the following questions within the existing scholarship of the medical sociology of confinement and incarceration: In what ways are experiences of confinement alike for older adults living in prisons and for those living in nursing homes, and what do these similarities/differences imply about aging, disabled, and economically unproductive bodies as "deviant" and subsequently "criminal" as the traditional definition of the carceral space expands? Participant responses across the nursing home and prison settings fit into three categories, including "home as historical/home as negation," "institution as escape," and "self as non-human/self as non-agent." As a result, there exist thematic consistencies amidst the subjective experiences of older adults across settings of confinement that argue for a shared "criminality" socially assigned to an aging body.

Plasma BDNF levels associate with Pittsburgh compound B binding in the brain.

BACKGROUND: Brain-derived neurotrophic factor (BDNF) plays an important role in Alzheimer's disease (AD) and other neurodegenerative disorders. BDNF function is adversely affected by amyloid beta (Aß) in AD. BDNF levels in brain and peripheral tissues are lower in patients with AD and MCI, than in controls. Here we examined the association between plasma levels of BDNF and amyloid deposition in the brain measured with Pittsburgh Compound B (PiB). METHOD: Our dataset consisted of 18 AD, 56 mild cognitive impairment (MCI) and 3 normal control (NC) Alzheimer's Disease Neuroimaging Initiative-1 (ADNI1) subjects with available [11C] PiB and peripheral blood protein data. MRI-coregistered PET data was smoothed with a 15 mm kernel and mapped onto 3D hemispheric models using the warping deformations computed in cortical pattern matching of the associated MRI scans. We applied linear regression to examine in 3D the associations between BDNF and PiB SUVR, while adjusting for age and sex. We used permutation statistics thresholded at p<0.01 for multiple comparisons correction. RESULTS: Plasma BDNF levels showed significant negative associations with left greater than right amyloid burden in the lateral temporal, inferior parietal, inferior frontal, anterior and posterior cingulate, and orbitofrontal regions (left pcorrected=0.03). CONCLUSIONS: As hypothesized, lower plasma levels of BDNF were significantly associated with widespread brain amyloidosis.