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The existence of beta-amyloid [Aβ] peptides in the brain has been regarded as the most archetypal biomarker of Alzheimer's disease [AD].
Traditionally, the brain has been regarded as an immunologically privileged site [ 2, 4, 5, 27, 28].
In this regard, the presence of activated microglia in the PD brain has been regarded as a sensitive index of neuropathological changes that are present not only in SN but also in other brain regions such hippocampus and cortex (Imamura et al., 2003).
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For many years, the brain had been regarded as an immune-privileged organ because of an old tenet which stated that no classical immune activation or inflammation could take place intrathecally.
The amygdala is a key structure of the emotional brain and has been regarded a socio-emotional relevance detector [6].
Temperature measured at the tip of the thermistor in situ and irrespective of brain site has been regarded as 'brain' temperature for the purposes of this systematic review but issues regarding the site of measurement and differences in temperature values at damaged versus undamaged sites could have a bearing on the brain temperature reading.
The BBB is a primary hindrance towards drug development of brain and it has been regarded as one of the most important obstacle which limits the future growth of neurotherapeutics.
AD has been regarded as an unsolved, irreversible, and incurable brain neuron degeneration.
This activity has been regarded as protective in conditions (such as cerebral ischemia) in which the glucose supply to the brain is reduced [ 43].
For this reason, SPARC has been regarded as an enhancer of the capability of glioblastomas to localise in multiple sites of the brain (Schultz et al, 2002).
Sumatriptan, a relatively hydrophilic triptan, based on several animal studies has been regarded to be unable to cross the blood brain barrier (BBB).
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