Background: Severe traumatic brain injury (TBI) is a major cause of morbidity and mortality. Reduction of thalamic volumes were seen in upto 80% of patients who survived for more than 3 months after TBI. However, the same may not be true in patients who died earlier following TBI. Aims: To to study the thalamus for evidence of any injury in short term survivors of TBI (<5 days) using immunohistochemistry to look for evidence of acute thalamic injury. Materials and Methods: A cross sectional prospective study was done in which autopsy specimens of short term survivors of TBI (<5 days) were studied for histopathological changes. Results: A total of 16 patients with a mean age of 37.8 years were included in the study. CT scan revealed acute subdural haematoma in 10, contusions in 4 patients, extradural haematoma and depressed fracture in 1 each, and diffuse axonal injury in 1 patient. Seven patients required surgery in the form of a decompressive hemicraniectomy. The histopathological analysis of the bilateral thalami showed evidence of congestion of the cerebral capillaries in 8 patients. Axonal retraction balls were seen in 8 patients, myelin breakdown products were seen in 14 patients and axonal swelling was seen in 14 patients. Conclusions: Thalamic injury is universal in the setting of severe TBI in patients who have decreased survival and may be a significant factor for the poor outcome in these patients.

Murine transgenic models of Alzheimer's disease (Tg-AD) have been useful to analyze the contribution of beta-amyloid precursor protein (beta APP), A beta 42 peptide deposition, and the proinflammatory mechanisms that characterize Alzheimer-type neuropathology. In this report, we have studied the levels of beta APP, A beta 40 and A beta 42 peptide, as well as the innate immune and inflammatory response-regulator complement factor H in the brain and retina in four different Tg-AD models including Tg2576, PSAPP, 3xTg-AD, and 5xFAD. Aged, symptomatic 5xFAD mice showed the highest retinal abundance of A beta 42 peptides and the highest deficits in complement factor H. This may be a useful model to study the mechanisms of amyloid-mediated inflammatory degeneration. The superior colliculus and retina obtained from late-stage Alzheimer's disease revealed upregulated amyloidogenic and inflammatory signaling along the anteroposterior axis of the retinal-primary visual cortex pathway. NeuroReport 22:623-627 (C) 2011 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.