Journal Article Localized accumulation of tau without amyloid-beta in aged brains measured with [11C]PBB3 and [11C]PiB positron emission tomography

Kikukawa, Takayuki  ,  Saito, Haruna  ,  Hasegawa, Itsuki  ,  Takeuchi, Jun  ,  Takeda, Akitoshi  ,  Kawabe, Koji  ,  Wada, Yasuhiro  ,  Mawatari, Aya  ,  Watanabe, Yasuyoshi  ,  Kitamura, Soichiro  ,  Shimada, Hitoshi  ,  Higuchi, Makoto  ,  Suhara, Tetsuya  ,  Itoh, Yoshiaki

Objective Different regional specificity in tau accumulation is well known in Alzheimer’s disease (AD) brains. However, little is known about such distribution in aging brains and mild cognitive impairment (MCI) brains.Methods Cognitive functions and regional accumulation of tau and amyloid (A) were evaluated in 13 healthy controls (HCs), 3 patients with MCI, and 4 AD patients. Tau and A accumulation was semi-quantitatively measured with positron emission tomography (PET) using [11C]pyridinyl-butadienyl-benzothiazole 3 (PBB3) and [11C]Pittsburgh compound-B (PiB).Results Age-dependent accumulation of tau was found in all predetermined regions characteristic of AD, especially in the parahippocampal gyrus, lateral temporal cortex, frontal cortex, and posterior cingulate gyrus, where age-dependency was statistically significant. In contrast, age-dependency in accumulation of A was not observed in most regions assessed in HC. Moreover, the accumulation of tau in regions characteristic of AD in MCI patients were higher than that in HC, whereas tau accumulation was highest and statistically significant in AD patients. Unlike HC, the accumulation of tau was accompanied by that of Ain patients with MCI and AD. Conclusion Mild and age-dependent accumulation of tau without A was found in AD-related areas in aging brains. Considering age as a major risk for AD, higher accumulation of tau may trigger the neurodegenerative process of AD.

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