Research Laboratories
MOLECULAR NEUROSCIENCE (Kanae Ando, Taro Saito, Akiko Asada)
Summary
A person's ability to be moved by beautiful sights and wonderful music, to remember enjoyable things, or to create new concepts rely on a complex network of nerve cells in the brain. Unlike other cells in the body, these neurons are not replaced throughout life, but age with the individual brain owner. When these nerve cells die due to diseases such as Alzheimer's disease, dementia and cognitive decline usually follow. How can we prevent age-related loss of neuronal function, minimize disease risk, and maintain brain function throughout a person's life?
To answer these questions, we use a variety of methods, including molecular and cell behavioral biology, mice and Drosophila disease models, imaging, experiments and gene expression analysis. Our research can help us understand the complexities of brain function and aging, ultimately allowing us to develop future preventative and therapeutic strategies.
Our current research themes include the following:
- Brain anti-aging with focus on feeding and intracellular energy metabolism
- Pathogenic mechanisms of age-dependent neurodegenerative diseases
- Roles of mitochondria in brain aging and disease
We are always looking for enthusiastic graduate students. Don't hesitate to contact us if you are interested in doing research with us!
Department Laboratory Page
Molecular Neuroscience Laboratory
Current Projects
(1) Brain anti-aging with focus on feeding and intracellular energy metabolism
Aging causes a decline in cognitive function such as memory, but what are the changes in neurons that trigger memory loss? We are looking for ways to reduce brain aging by focusing on age-related changes in energy metabolism within the brain's neurons. We are also interested in how diet and glucose metabolism in brain neurons affect processes that causes them to age, especially since dietary changes such as caloric restriction has been found to increase lifespan.
(2) Pathogenic mechanisms of age-dependent neurodegenerative diseases
The mechanisms underlying the onset and progression of neurodegenerative disease the develop in old age, such as Alzheimer's disease, remain largely unknown. As such, there is currently no fundamental cure for these diseases. A protein called tau is thought to accumulate in the brain in these diseases and cause neuronal cell death. Normally, tau regulates the stability of microtubules (an essential component of the cytoskeleton) in axons. However, in diseased brains, tau undergoes phosphorylation and other modifications that cause changes in its structure that eventually lead to build up abnormally. Our goal is to elucidate the molecular mechanisms that cause tau alterations in the diseased brain and identify strategies to alleviate tau-induced neuronal cell death.
(3) Roles of mitochondria in brain aging and disease
Mitochondria are cell organelles that are responsible for generating majority of the energy supply inside the cell. They also participate in important functions such a nucleic acid synthesis, lipid, iron, and urea metabolism, and cell-to-cell signaling. Because of their cell structure and function, neurons in the brain not only require a constant supply of large amounts of energy, they also need their mitochondria to be distributed far out into their long extending projections (axons) to support information transmission. Mitochondrial diseases caused by abnormalities in mitochondrial structure or intracellular transport have neurological symptoms, and these abnormalities may also be involved in the development of neurodegenerative diseases in old age. We are thus investigating the nature of age-related changes in the mitochondria and their contribution to increased risk of brain aging and neurodegenerative diseases. We are also looking at whether mitochondrial activation can alleviate the symptoms associated with mitochondrial diseases and the decline in brain function due to aging.
Staff Highlight
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Dr. Kanae Cono (安藤香奈絵) Professor | Dr. Taro Saito (斉藤太郎) Assistant Professor | Dr. Akiko Asada (淺田明子) Assistant Professor |
Email: | ||
k_ando[at]tmu.ac.jp | tasaito[at]tmu.ac.jp | a7203ki[at]tmu.ac.jp |
| Read more: | ||
Lab Information: Department Laboratory Page (Japanese ) | ||
Recent Publications
1. MARK4 regulates GLUT3 surface expression and neural glucose uptake
Sophia Limlingan, Ambika Krishnankutty, Akiko Asada, Kanae Ando, Taro Saito. Journal of Biochemistry , Aug 2026
Emilie L. Castranio, Merina Varghese, Elentina K. Argyrousi, Kuldeep Tripathi, Yong Huang, Akiko Asada, Linda Söderberg, Erin Bresnahan, David Lerner, Francesca Garretti, Hong Zhang, Jonathan van de Loo, Cheryl D. Stimpson, Ronan Talty, Charles Glabe, Efrat Levy, Minghui Wang, Marjan Ilkov, Toshiharu Suzuki, Kanae Ando, Bin Zhang, Lars Lannfelt, Brigitte Guérin, William D. Lubell, Shai Rahimipour, Dara L. Dickstein, Sam Gandy, Ottavio Arancio, Michelle E. Ehrlich. Alzheimer's & Dementia, 22:e71426, June 2026
3. Cyclin-dependent kinases in neurodegenerative disorders
Taro Saito, Kanae Ando, Protein serine/threonine kinases in neurodegenerative disorders (pp. 109–119). Academic Press. June 2026
4. 5-ALA/SFC Mitigates Tau Toxicity via Lowering Oxidative Stress in a Drosophila Model of Tau Toxicity
Arisa Tamura, Marie Noguchi, Naoko Nozawa, Emiko Suzuki, Kanae Ando. Life , 16 (5), 725, April 2026.
5. Axonal distribution of mitochondria maintains neuronal autophagy during aging via eIF2β
Kanako Shinno, Yuri Miura, Koichi M Iijima, Emiko Suzuki, Kanae Ando. eLife 13 :RP95576, Jan 2026
6. Therapeutic effects by the peptide drug of p3‐Alcß in AD mouse model
Toshiharu Suzuki, Haruka Saito, Shoichi Kinoshita, Kanae Ando, Saori Hata. Alzheimer's & Dementia , 21: e101763. Dec 2025.
7. Glial MARK2 Modulate Inflammatory Signaling and Protects Against Tau‐induced Neurodegeneration
Aoi Fukuchi, Taro Saito, Kanae Ando. Alzheimer's & Dementia , 21: e108155, Dec 2025.
8. Tau disrupts OXPHOS complexes and hyperpolarizes mitochondria
Arisa Tamura, Marie Noguchi, Taro Saito, Akiko Asada, Kanae Ando. Alzheimer's & Dementia , 21: e100654, Dec 2025
9. CCT4 promotes tunneling nanotube formation
Miyu Enomoto, Akiko Asada, Taro Saito, Kanae Ando. FEBS letters , 600: 39-47, October 2025
10. Glucose uptake in pigment glia suppresses Tau-induced inflammation and photoreceptor degeneration
Mikiko Oka, Sho Nakajima, Emiko Suzuki, Shinya Yamamoto, Kanae Ando. Dis Model Mech, 18(4): dmm052057, April 2025
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