8 research outputs found
Behavioral Stress Fails to Accelerate the Onset and Progression of Plaque Pathology in the Brain of a Mouse Model of Alzheimer's Disease
âIdentify-to-rejectâ: A specific strategy to avoid false memories in the DRM paradigm
Non-pharmacological interventions and neuroplasticity in early stage Alzheimer's disease
Reconceptualization of translocator protein as a biomarker of neuroinflammation in psychiatry
Reconceptualization of translocator protein as a biomarker of neuroinflammation in psychiatry
A great deal of interest in psychiatric research is currently centered upon the pathogenic role of inflammatory processes. Positron emission tomography (PET) using radiolabeled ligands selective for the 18 kDa translocator protein (TSPO) has become the most widely used technique to assess putative neuroimmune abnormalities in vivo. Originally used to detect discrete neurotoxic damages, TSPO has generally turned into a biomarker of âneuroinflammationâ or âmicroglial activationâ. Psychiatric research has mostly accepted these denotations of TSPO, even if they may be inadequate and misleading under many pathological conditions. A reliable and neurobiologically meaningful diagnosis of âneuroinflammationâ or âmicroglial activationâ is unlikely to be achieved by the sole use of TSPO PET imaging. It is also very likely that the pathological meanings of altered TSPO binding or expression are disease-specific, and therefore, not easily generalizable across different neuropathologies or inflammatory conditions. This difficulty is intricately linked to the varying (and still ill-defined) physiological functions and cellular expression patterns of TSPO in health and disease. While altered TSPO binding or expression may indeed mirror ongoing neuroinflammatory processes in some cases, it may
reflect other pathophysiological processes such as abnormalities in cell metabolism, energy production and oxidative stress in others. Hence, the increasing popularity of TSPO PET imaging has paradoxically introduced substantial uncertainty regarding the nature and meaning of neuroinflammatory processes and microglial activation in psychiatry, and likely in other neuropathological conditions as well. The ambiguity of conceiving TSPO simply as a biomarker of âneuroinflammationâ or âmicroglial activationâ calls for alternative interpretations and complimentary approaches. Without the latter, the ongoing scientific efforts and excitement surrounding the role of the neuroimmune system in psychiatry may not turn into therapeutic hope for affected individuals