We investigate neuron–glia–vascular interactions in neurodegenerative diseases, with a focus on mechanisms underlying axon–myelin pathology and neuroimmune regulation. Our work integrates human brain proteomics, iPSC-based modeling, in vivo imaging, and genetic tools to uncover disease mechanisms and identify therapeutic targets.

• Oligodendrocyte and myelin-axonal degeneration
• Neurovascular and blood–brain barrier dysfunction
• Neuroimmune signaling in Alzheimer’s disease and related disorders
• Advanced tool development: Multi-modal integration of proteomics and imaging, iPSC-based disease modeling and AAV tool development

2026 - 2029    BrightFocus Alzheimer's Disease Research Standard Award, BrightFocus Foundation 

2025 - 2026    Pilot Project Award, Carol and Gene Ludwig Program for the Study of Neuroimmune Interactions in Dementia

2023 - 2026    Alzheimer's Association Research Fellowship, Alzheimer's Association

2023 – 2024   EMBL-CPP Fellowship, European Molecular Biology Laboratory (EMBL)

2021 - 2023    BrightFocus Postdoc Fellowship in Alzheimer's Research, BrightFocus Foundation

1. Y. Cai†, I.P. Sousa∗, M. Slobodyanyuk∗, F. Chen∗, T. Huynh, P. Tang, L. Fuentes, A. Braker, R. Welch, A. Huttner, L. Tong, P. Yuan, T.T. Lam, A.C. Nairn, E. Petsalaki, J. Reimand, J. Grutzendler†. Myelin–axon interface vulnerability in Alzheimer’s disease revealed by subcellular proteomics and imaging of human and mouse brain. (2025) Nature Neuroscience. doi: 10.1038/s41593-025-01973-8. 

2. Y. Cai†, J. Kanyo, R. Wilson, S. Bathla, P. Cardozo, L. Tong, S. Qin, L.A. Fuentes, I.Pinheiro-de-Sousa, T. Huynh, L. Sun, M. Mohammad, Z. Tian, H. Gan, A. Braker, K. Trinh, A. Huttner, T. T. Lam, E. Petsalaki, K. J. Brennand, A.C. Nairn, J. Grutzendler†. Subcellular proteomics and iPSC modeling uncover reversible mechanisms of axonal pathology in Alzheimer’s disease. (2025) Nature Aging. doi: 10.1038/s43587-025-00823-3. 

3. P. Yuan, M. Zhang, L. Tong, T.M. Morse, R.A. McDougal, H. Ding, D. Chan, Y. Cai, J. Grutzendler. PLD3 affects axonal spheroids and network defects in Alzheimer’s disease. Nature. 612, 328–337 (2022).

4. J. Mukai, E. Canavo, Z. Sun, A. Diamantopoulou, P. Thakur, C. Chang, Y. Cai, S. Lomvardas, A. Takata, B. Xu, J.A. Gogos. Recapitulation and reversal of schizophreniarelated phenotypes in Setd1a-deficient mice. Neuron. 104 (3): 471-487 (2019).

5. J. Guo, Y. Cai, X. Ye, N. Ma, Y. Wang, B. Yu, J. Wan. Regulation of neurite outgrowth by miR-409-5p is involved in Alzheimer’s disease development. Front. Neurosci. 13, 2164 (2019).

6. Y. Cai, J. Wan. Competing endogenous RNA regulations in neurodegenerative disorders: current challenges and emerging insights. Front. Mol. Neurosci. 11, 370 (2018).

7. Y. Cai, Z. Sun, H. Jia, H. Luo, X. Ye, Q. Wu, X. Yi, W. Zhang, J. Wan. Rpph1 upregulates CDC42 expression and promotes hippocampal neuron dendritic spine formation by competing with miR-330-5p. Front. Mol. Neurosci. 10, 27 (2017).

8. Y. Cai*, Z. Liang*, T. He, G. Zhang, J. Huang, X. Zeng. Augmenting LASSO regression with decision tree for identifying the correlation of genetic polymorphism and adverse events. IEEE International Conference on Bioinformatics and Biomedicine (BIBM), 355-360 (2013).