A5063257237- Alzheimer's disease research and treatments
- Dementia and Cognitive Impairment Research
- Receptor Mechanisms and Signaling
- Neuroinflammation and Neurodegeneration Mechanisms
- Photoreceptor and optogenetics research
- Functional Brain Connectivity Studies
- Neurological Disease Mechanisms and Treatments
- Cholinesterase and Neurodegenerative Diseases
- bioluminescence and chemiluminescence research
- Advanced Fluorescence Microscopy Techniques
- Bioinformatics and Genomic Networks
The University of Tokyo
2020-2024
The genetic associations of TREM2 loss-of-function variants with Alzheimer disease (AD) indicate the protective roles microglia in AD pathogenesis. Functional deficiencies disrupt microglial clustering around amyloid β (Aβ) plaques, impair their transcriptional response to Aβ, and worsen neuritic dystrophy. However, molecular mechanism underlying these phenotypes remains unclear. In this study, we investigated pathological role another risk gene, INPP5D, encoding a phosphoinositide...
The aberrant metabolism of amyloid β peptide (Aβ) has been implicated in the etiology Alzheimer disease (AD). Aβ is produced via sequential cleavage precursor protein (APP) by β- and γ-secretases. However, precise regulatory mechanism generation still remains unclear. To gain a better understanding molecular production, we established genetic screening method based on CRISPR/Cas9 system to identify novel regulators production. We successfully identified calcium integrin-binding 1 (CIB1) as...
Abstract L-Lactate, traditionally recognized as a waste product of metabolism, is now appreciated key intercellular energy currency in mammals. To enable investigations shuttling L-lactate, we have previously reported eLACCO1.1, green fluorescent genetically encoded biosensor for extracellular L-lactate. eLACCO1.1 enables cellular resolution imaging L-lactate cultured mammalian cells and brain tissue. However, spectrally overlaps with commonly used optical biosensors actuators, limiting its...
<title>Abstract</title> The transient build-up of L-lactate in tissue is associated with acidosis, as occurs during hypoxia, and traditionally viewed deleterious1–3. However, recent studies contradict this view by demonstrating L-lactate's vital role an intercellular interorgan exchangeable fuel4. As one example, the astrocyte-to-neuron lactate shuttle (ANLS) hypothesis proposes that neurons import from astrocytes via extracellular space to produce adenosine triphosphate (ATP) sustain...