Its presence has been documented in various brain regions where significant changes are associated with aging [13], [19].
In the neuronopathic variants, GC and glucosylsphingosine (GS) accumulations have been documented in the brain (6– 8).
These structural abnormalities have been previously observed in the post-mortem brain of dyslexic individuals (Galaburda et al. 1985) and have also been documented in rat brains where Dyx1c1 has been knocked-down by RNA interference (RNAi) (Rosen et al. 2007).
Iron accumulation has also been documented in the brains of migraine patients [23].
Damage to brain stem nuclei is a main pathological findings in infants who died by asphyxia [6] and disruption in the neuron morphology of these nuclei has been documented in autistic brains [7].
The increased expression and activity of iNOS and COX-2 have been documented in various tissues (brain, skeletal muscle, lung, and cardiac tissue) of rodent and porcine models of neonatal sepsis when initiated using Escherichia coli, GBS or LPS [ 41, 50- 57].
Similar to PD, neurodegeneration has been documented in post-mortem brains of manganism patients and therefore may be a feature of the terminal pathological stage and may not be related to early symptoms (Perl and Olanow, 2007).
The imaging potentialities of 11C-methionine as an oncological PET tracer have already been documented in different malignancies like brain tumours, breast cancer and head and neck tumours [17, 18, 19].
The capability of Mel to enhance Akt activation in the setting of I/R has been documented in several organs including brain [ 43] and liver [ 44] but is not yet proven in kidney.
