Leyla Anne Akay
- Neurology top 2%
- Neuroinflammation and Neurodegeneration Mechanisms 4
- Barrier Structure and Function Studies 1
- Developmental Neuroscience top 5%
- Neurogenesis and neuroplasticity mechanisms 2
- Biological Psychiatry top 10%
- Physiology top 10%
- Alzheimer's disease research and treatments 3
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- Single-cell and spatial transcriptomics 2
- S100 Proteins and Annexins 2
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- Cholesterol and Lipid Metabolism 1
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- Neural dynamics and brain function 1
- Co-authors
- Li‐Huei TsaiManolis KellisJulia Maeve BonnerHansruedi MathysJosé Dávila-VelderrainYuan-Ta LinAgnese GraziosiBlerta Milo
- Partner nations
- United StatesItalyCanada
In The Last Decade
Leyla Anne Akay
10 papers receiving 785 citations
Hit Papers
Peers
Comparison fields: 5 of 95
- Neurology 317
- Developmental Neuroscience 97
- Biological Psychiatry 52
- Physiology 276
- Cellular and Molecular Neuroscience 131
Countries citing papers authored by Leyla Anne Akay
This map shows the geographic impact of Leyla Anne Akay'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 Leyla Anne Akay with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Leyla Anne Akay more than expected).
Fields of papers citing papers by Leyla Anne Akay
This network shows the impact of papers produced by Leyla Anne Akay. 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 Leyla Anne Akay. The network helps show where Leyla Anne Akay may publish in the future.
Co-authorship network
The 25 scholars most cited alongside Leyla Anne Akay, linked wherever they have co-authored with each other. Click a name or a connecting line to browse the papers they share.
All Works
| # | Work | ||
|---|---|---|---|
| 1 | 2025 | 0 | |
| 2 | Single-cell multiregion dissection of Alzheimer’s diseasebreakdown → | 2024 | 83 |
| 3 | 2023 | 72 | |
| 4 | 2023 | 1 | |
| 5 | APOE4 disrupts intracellular lipid homeostasis in human iPSC-derived gliabreakdown → | 2021 | 197 |
| 6 | 2021 | 87 | |
| 7 | 2021 | 4 | |
| 8 | 2020 | 182 | |
| 9 | 2020 | 57 | |
| 10 | 2020 | 24 | |
| 11 | 2018 | 86 |
About Leyla Anne Akay
Leyla Anne Akay is a scholar working on Neurology, Developmental Neuroscience and Biological Psychiatry, having authored 11 papers that have together received 793 indexed citations. Recurring topics across this work include Neuroinflammation and Neurodegeneration Mechanisms (4 papers), Alzheimer's disease research and treatments (3 papers), Single-cell and spatial transcriptomics (2 papers), S100 Proteins and Annexins (2 papers), Neurogenesis and neuroplasticity mechanisms (2 papers), Barrier Structure and Function Studies (1 paper), Cholesterol and Lipid Metabolism (1 paper) and Neural dynamics and brain function (1 paper). The work is most often cited by research in Neurology (317 citations), Developmental Neuroscience (97 citations) and Biological Psychiatry (52 citations). Leyla Anne Akay has collaborated with scholars based in United States, Italy and Canada. Frequent co-authors include Li‐Huei Tsai, Manolis Kellis, Julia Maeve Bonner, Hansruedi Mathys, José Dávila-Velderrain, Yuan-Ta Lin, Agnese Graziosi, Blerta Milo, Priyanka Narayan and Grzegorz Sienski. Their work appears in journals such as Nature, Nature Medicine and Genes & Development.
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.