No abstract

A lack of coupling between microglial activation and amyloid deposits may indicate that Aβ accumulation shown by [(11)C]PIB is not always the primary cause of microglial activation, but rather the negative correlation present in the PCC suggests that microglia can show higher activation during the production of Aβ in early AD.

The current results indicated that an extrastriatal spreading of microglial activation reflects one of PD pathophysiology occurring at an early stage.

The presence of activated microglia in the brains of healthy elderly people is a matter of debate. We aimed to clarify the degree of microglial activation in aging and dementia as revealed by different tracers by comparing the binding potential (BP ND ) in various brain regions using a first-generation translocator protein (TSPO) tracer [11 C](R)PK11195 and a second-generation tracer [11 C]DPA713. The BP ND levels, estimated using simplified reference tissue models, were compared among healthy young and elderly individuals and patients with Alzheimer's disease (AD) and were correlated with clinical scores. An analysis of variance showed category-dependent elevation in levels of [ 11 C]DPA713 BP ND in all brain regions and showed a significant increase in the AD group, whereas no significant changes among groups were found when

GABA is the main inhibitory neurotransmitter in the adult brain. However, GABAergic transmission is depolarizing during early postnatal development, suggesting that changes in the expression of cation-Cl- co-transporters regulating neuronal Cl- homeostasis underlie the ontogeny of GABAergic functions. The developmental changes in the expressions of Cl- co-transporter mRNAs in the neocortex were in opposite directions for NKCC1 (Cl- uptake) and KCC2 (Cl- extrusion). In the newborn, NKCC1 mRNA expression was highest in ventricular zone followed by cortical plate, and then by Layer V/VI, while the reverse was true for KCC2 mRNA. The [Cl-]i levels were in the same rank order as for NKCC1 mRNA. Thus, the ontogeny of Cl- homeostasis in neocortical neurons could be regulated via the differential expression of NKCC1 and KCC2.