Kanae Ando

1.9k total citations
49 papers, 1.3k citations indexed

About

Kanae Ando is a scholar working on Molecular Biology, Physiology and Cell Biology. According to data from OpenAlex, Kanae Ando has authored 49 papers receiving a total of 1.3k indexed citations (citations by other indexed papers that have themselves been cited), including 28 papers in Molecular Biology, 28 papers in Physiology and 15 papers in Cell Biology. Recurrent topics in Kanae Ando's work include Alzheimer's disease research and treatments (27 papers), Neuroscience and Neuropharmacology Research (8 papers) and Cholinesterase and Neurodegenerative Diseases (7 papers). Kanae Ando is often cited by papers focused on Alzheimer's disease research and treatments (27 papers), Neuroscience and Neuropharmacology Research (8 papers) and Cholinesterase and Neurodegenerative Diseases (7 papers). Kanae Ando collaborates with scholars based in Japan, United States and Iran. Kanae Ando's co-authors include Koichi Iijima, Yutaka Kirino, Toshiharu Suzuki, James I. Elliott, Taro Saito, Paul Greengard, Angus C. Nairn, Shin‐ichi Hisanaga, Shizu Takeda and Akiko Asada and has published in prestigious journals such as Journal of Biological Chemistry, Journal of Neuroscience and Nature Neuroscience.

In The Last Decade

Kanae Ando

45 papers receiving 1.3k citations

Peers — A (Enhanced Table)

Peers by citation overlap · career bar shows stage (early→late) cites · hero ref

Name h Career Trend Papers Cites
Kanae Ando Japan 19 856 681 309 273 185 49 1.3k
Celina Zerbinatti United States 17 976 1.1× 619 0.9× 200 0.6× 393 1.4× 173 0.9× 24 1.5k
A. L. Schwarzman Russia 14 637 0.7× 656 1.0× 211 0.7× 196 0.7× 151 0.8× 38 1.1k
Paul H. Wen United States 14 674 0.8× 733 1.1× 216 0.7× 369 1.4× 222 1.2× 24 1.4k
Jordana L. Meyerson United States 7 746 0.9× 522 0.8× 152 0.5× 291 1.1× 219 1.2× 14 1.2k
Charlotte Bauer France 15 733 0.9× 529 0.8× 219 0.7× 241 0.9× 188 1.0× 20 1.1k
Hiroshi Hasegawa Japan 14 674 0.8× 668 1.0× 243 0.8× 253 0.9× 167 0.9× 22 1.2k
Nobumasa Takasugi Japan 14 1.0k 1.2× 979 1.4× 412 1.3× 267 1.0× 292 1.6× 35 1.6k
David E. Merriam United States 5 757 0.9× 570 0.8× 250 0.8× 341 1.2× 183 1.0× 5 1.1k
Philip J. Dolan United States 10 574 0.7× 666 1.0× 138 0.4× 215 0.8× 208 1.1× 14 1.1k
Misaki Sekiguchi Japan 11 964 1.1× 531 0.8× 147 0.5× 272 1.0× 262 1.4× 19 1.4k

Countries citing papers authored by Kanae Ando

Since Specialization
Citations

This map shows the geographic impact of Kanae Ando's research. It shows the number of citations coming from papers published by authors working in each country. You can also color the map by specialization and compare the number of citations received by Kanae Ando with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Kanae Ando more than expected).

Fields of papers citing papers by Kanae Ando

Since Specialization
Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Kanae Ando. Nodes represent research fields, and links connect fields that are likely to share authors. Colored nodes show fields that tend to cite the papers produced by Kanae Ando. The network helps show where Kanae Ando may publish in the future.

Co-authorship network of co-authors of Kanae Ando

This figure shows the co-authorship network connecting the top 25 collaborators of Kanae Ando. A scholar is included among the top collaborators of Kanae Ando based on the total number of citations received by their joint publications. Widths of edges represent the number of papers authors have co-authored together. Node borders signify the number of papers an author published with Kanae Ando. Kanae Ando is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

20 of 20 papers shown
1.
Nakajima, Sho, et al.. (2025). Glucose uptake in pigment glia suppresses Tau-induced inflammation and photoreceptor degeneration. Disease Models & Mechanisms. 18(4).
2.
Suzuki, Hirokazu, et al.. (2024). Mark4 ablation attenuates pathological phenotypes in a mouse model of tauopathy. Brain Communications. 6(3). fcae136–fcae136.
3.
Rajani, Vishaal, et al.. (2024). Hippocampal hyperphosphorylated tau-induced deficiency is rescued by L-type calcium channel blockade. Brain Communications. 6(2). fcae096–fcae096. 1 indexed citations
4.
5.
6.
Honda, Keiko, Hiroo Takahashi, Saori Hata, et al.. (2024). Suppression of the amyloidogenic metabolism of APP and the accumulation of Aβ by alcadein α in the brain during aging. Scientific Reports. 14(1). 2 indexed citations
7.
Saito, Taro, Akiko Asada, Takuya Ishii, et al.. (2023). 5-Aminolevulinic acid bypasses mitochondrial complex I deficiency and corrects physiological dysfunctions in Drosophila. Human Molecular Genetics. 32(16). 2611–2622. 2 indexed citations
8.
9.
Saito, Taro, Akiko Asada, Takuya Ishii, et al.. (2021). 5‐Aminolevulinic acid and sodium ferrous citrate ameliorate muscle aging and extend healthspan in Drosophila. FEBS Open Bio. 12(1). 295–305. 2 indexed citations
10.
Saito, Taro, Satoko Wada‐Kakuda, Saori Abe, et al.. (2021). Disulfide bond formation in microtubule-associated tau protein promotes tau accumulation and toxicity in vivo. Human Molecular Genetics. 30(21). 1955–1967. 29 indexed citations
11.
Kimura, Taeko, Tomoyasu Matsubara, Yuko Saito, et al.. (2021). Distinct phosphorylation profiles of tau in brains of patients with different tauopathies. Neurobiology of Aging. 108. 72–79. 19 indexed citations
12.
Saito, Taro, et al.. (2020). Microtubule affinity–regulating kinase 4 with an Alzheimer's disease-related mutation promotes tau accumulation and exacerbates neurodegeneration. Journal of Biological Chemistry. 295(50). 17138–17147. 30 indexed citations
13.
Saito, Taro, Ran Wei, Tetsuya Takano, et al.. (2019). The LMTK1-TBC1D9B-Rab11A Cascade Regulates Dendritic Spine Formation via Endosome Trafficking. Journal of Neuroscience. 39(48). 9491–9502. 26 indexed citations
14.
Kimura, Taeko, Seiji Shiozawa, Naruhiko Sahara, et al.. (2019). Tau isoform expression and phosphorylation in marmoset brains. Journal of Biological Chemistry. 294(30). 11433–11444. 32 indexed citations
15.
Takahashi, Miyuki, Yuki Kobayashi, Kanae Ando, Yumiko Saito, & Shin‐ichi Hisanaga. (2019). Cyclin-dependent kinase 5 promotes proteasomal degradation of the 5-HT1A receptor via phosphorylation. Biochemical and Biophysical Research Communications. 510(3). 370–375. 5 indexed citations
16.
Saito, Taro, et al.. (2019). Cdk5 increases MARK4 activity and augments pathological tau accumulation and toxicity through tau phosphorylation at Ser262. Human Molecular Genetics. 28(18). 3062–3071. 35 indexed citations
17.
Saito, Taro, Yosuke Ohtake, Akiko Asada, et al.. (2018). S6K/p70S6K1 protects against tau-mediated neurodegeneration by decreasing the level of tau phosphorylated at Ser262 in a Drosophila model of tauopathy. Neurobiology of Aging. 71. 255–264. 9 indexed citations
18.
Kimura, Taeko, Tomohiro Miyasaka, Aki Shimozawa, et al.. (2017). Isoform-independent and -dependent phosphorylation of microtubule-associated protein tau in mouse brain during postnatal development. Journal of Biological Chemistry. 293(5). 1781–1793. 37 indexed citations
19.
Shinano, Takuro, Kanae Ando, Keiichi Okazaki, & Mitsuru Osaki. (2006). Developmental changes of plant affecting primary photosynthate distribution in rice leaves. Photosynthetica. 44(4). 591–598. 4 indexed citations
20.
Ando, Kanae, et al.. (1975). [Clinical observation on endometriosis related with sterility and habitual abortion].. PubMed. 20(2). 34–9. 1 indexed citations

Rankless uses publication and citation data sourced from OpenAlex, an open and comprehensive bibliographic database. While OpenAlex provides broad and valuable coverage of the global research landscape, it—like all bibliographic datasets—has inherent limitations. These include incomplete records, variations in author disambiguation, differences in journal indexing, and delays in data updates. As a result, some metrics and network relationships displayed in Rankless may not fully capture the entirety of a scholar's output or impact.

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