ABSTRACT
We applied optimised voxel based morphometry (VBM) to brain MRIs from autopsy proven cases of tau positive frontotemporal lobar degeneration (FTLD-T, n = 6), ubiquitin and TDP-43 positive/tau negative FTLD (FTLD-U, n = 8) and cognitively normal controls (n = 61). The analysis revealed that FTLD-T and FTLD-U both show atrophy in the frontal cortex and striatum, but striatal atrophy is more severe in FTLD-T. Manual region of interest tracing of caudate and putamen volumes confirmed the VBM findings. These anatomical differences may help distinguish between FTLD spectrum pathological subtypes in vivo.
Subject(s)
Dementia/metabolism , Dementia/pathology , Magnetic Resonance Imaging , Ubiquitin/metabolism , tau Proteins/metabolism , Aged , Atrophy/pathology , Autopsy , Caudate Nucleus/anatomy & histology , Dementia/complications , Dementia/diagnosis , Dementia/etiology , Female , Humans , Male , Neuropsychological Tests , Putamen/anatomy & histology , Severity of Illness IndexABSTRACT
To better define the anatomic distinctions between Alzheimer's disease (AD) and frontotemporal lobar degeneration (FTLD), we retrospectively applied voxel-based morphometry to the earliest magnetic resonance imaging scans of autopsy-proven AD (N = 11), FTLD (N = 18), and controls (N = 40). Compared with controls, AD patients showed gray matter reductions in posterior temporoparietal and occipital cortex; FTLD patients showed atrophy in medial prefrontal and medial temporal cortex, insula, hippocampus, and amygdala; and patients with both disorders showed atrophy in dorsolateral and orbital prefrontal cortex and lateral temporal cortex (P(FWE-corr) < .05). Compared with FTLD, AD patients had decreased gray matter in posterior parietal and occipital cortex, whereas FTLD patients had selective atrophy in anterior cingulate, frontal insula, subcallosal gyrus, and striatum (P < .001, uncorrected). These findings suggest that AD and FTLD are anatomically distinct, with degeneration of a posterior parietal network in AD and degeneration of a paralimbic fronto-insular-striatal network in FTLD.
Subject(s)
Alzheimer Disease/pathology , Brain/pathology , Dementia/pathology , Image Processing, Computer-Assisted , Imaging, Three-Dimensional , Magnetic Resonance Imaging , Aged , Aged, 80 and over , Alzheimer Disease/diagnosis , Amygdala/pathology , Atrophy , Cerebral Cortex/pathology , Corpus Striatum/pathology , Dementia/diagnosis , Diagnosis, Differential , Dominance, Cerebral/physiology , Female , Gyrus Cinguli/pathology , Hippocampus/pathology , Humans , Lewy Body Disease/diagnosis , Lewy Body Disease/pathology , Male , Middle AgedABSTRACT
Glucagon's effect on the placenta was studied in cultured human term trophoblast and in homogenized term and first-trimester placentas. In studies with cultured term trophoblast, glucagon stimulated the generation of cyclic AMP and estradiol secretion and inhibited placental lactogen secretion. Incubation of homogenates of term and of first-trimester placenta with 0.5 mM dibutyryl cAMP revealed a marked decrease of pyruvate kinase activity. Glucagon produced a similar decrease in first-trimester homogenates, but failed to affect term placentas. The present demonstration of the placenta as a target tissue for glucagon suggests an active contribution of the trophoblast to energy metabolism during pregnancy.
