Ola Philipson

545 total citations
9 papers, 417 citations indexed

About

Ola Philipson is a scholar working on Physiology, Molecular Biology and Cellular and Molecular Neuroscience. According to data from OpenAlex, Ola Philipson has authored 9 papers receiving a total of 417 indexed citations (citations by other indexed papers that have themselves been cited), including 7 papers in Physiology, 6 papers in Molecular Biology and 3 papers in Cellular and Molecular Neuroscience. Recurrent topics in Ola Philipson's work include Alzheimer's disease research and treatments (7 papers), Dementia and Cognitive Impairment Research (2 papers) and Prion Diseases and Protein Misfolding (2 papers). Ola Philipson is often cited by papers focused on Alzheimer's disease research and treatments (7 papers), Dementia and Cognitive Impairment Research (2 papers) and Prion Diseases and Protein Misfolding (2 papers). Ola Philipson collaborates with scholars based in Sweden, United States and Finland. Ola Philipson's co-authors include Lars Nilsson, Lars Lannfelt, Anna Lord, P.W. O’Callaghan, Astrid Gumucio, Per Hammarström, K. Peter R. Nilsson, Hannu Kalimo, Martin Ingelsson and Tommie Olofsson and has published in prestigious journals such as FEBS Letters, Neuroscience and American Journal Of Pathology.

In The Last Decade

Ola Philipson

9 papers receiving 408 citations

Peers

Ola Philipson

PHYSI

MB

NEURO

CMN

CTM

Astrid Gumucio Sweden

Orgeta Zejneli France

Jasmin Mahler Germany

Levi M. Smith United States

Jean-Noël Octave Belgium

Claire V. Cella United Kingdom

Tina L. Tekirian United States

Laurel Vana United States

Diana S. Himmelstein United States

Inga Volkmann Sweden

Astrid Gumucio Sweden

Ola Philipson

240 ×0.8

PHYSI

139 ×0.8

MB

86 ×0.9

NEURO

100 ×1.1

CMN

60 ×1.0

CTM

Citations per year, relative to Ola Philipson Ola Philipson (= 1×) peers Astrid Gumucio

Countries citing papers authored by Ola Philipson

Since Specialization

Citations

This map shows the geographic impact of Ola Philipson'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 Ola Philipson with the expected number of citations based on a country's size and research output (numbers larger than one mean the country cites Ola Philipson more than expected).

Fields of papers citing papers by Ola Philipson

Since Specialization

Physical SciencesHealth SciencesLife SciencesSocial Sciences

This network shows the impact of papers produced by Ola Philipson. 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 Ola Philipson. The network helps show where Ola Philipson may publish in the future.

Co-authorship network of co-authors of Ola Philipson

This figure shows the co-authorship network connecting the top 25 collaborators of Ola Philipson. A scholar is included among the top collaborators of Ola Philipson 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 Ola Philipson. Ola Philipson is excluded from the visualization to improve readability, since they are connected to all nodes in the network.

All Works

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9 of 9 papers shown

1.

Kalimo, Hannu, Maciej Łałowski, Nenad Bogdanović, et al.. (2013). The Arctic AβPP mutation leads to Alzheimer’s disease pathology with highly variable topographic deposition of differentially truncated Aβ. Acta Neuropathologica Communications. 1(1). 60–60. 38 indexed citations

2.

Magnusson, Kristina, Dag Sehlin, Stina Syvänen, et al.. (2013). Specific Uptake of an Amyloid-β Protofibril-Binding Antibody-Tracer in AβPP Transgenic Mouse Brain. Journal of Alzheimer s Disease. 37(1). 29–40. 75 indexed citations

3.

Lord, Anna, Ola Philipson, Therése Klingstedt, et al.. (2011). Observations in APP Bitransgenic Mice Suggest that Diffuse and Compact Plaques Form via Independent Processes in Alzheimer's Disease. American Journal Of Pathology. 178(5). 2286–2298. 33 indexed citations

4.

Philipson, Ola, Anna Lord, Maciej Łałowski, et al.. (2011). The Arctic amyloid-β precursor protein (AβPP) mutation results in distinct plaques and accumulation of N- and C-truncated Aβ. Neurobiology of Aging. 33(5). 1010.e1–1010.e13. 31 indexed citations

5.

Philipson, Ola, Anna Lord, Astrid Gumucio, et al.. (2010). Animal models of amyloid‐β‐related pathologies in Alzheimer’s disease. FEBS Journal. 277(6). 1389–1409. 80 indexed citations

6.

Hånell, Anders, Fredrik Clausen, Maria Björk, et al.. (2010). Genetic Deletion and Pharmacological Inhibition of Nogo-66 Receptor Impairs Cognitive Outcome after Traumatic Brain Injury in Mice. Journal of Neurotrauma. 27(7). 1297–1309. 33 indexed citations

7.

Marklund, Niklas, Diego M. Morales, Fredrik Clausen, et al.. (2009). Functional outcome is impaired following traumatic brain injury in aging Nogo-A/B-deficient mice. Neuroscience. 163(2). 540–551. 33 indexed citations

8.

Philipson, Ola, Lars Lannfelt, & Lars Nilsson. (2009). Genetic and pharmacological evidence of intraneuronal Aβ accumulation in APP transgenic mice. FEBS Letters. 583(18). 3021–3026. 19 indexed citations

9.

Philipson, Ola, Per Hammarström, K. Peter R. Nilsson, et al.. (2008). A highly insoluble state of Aβ similar to that of Alzheimer's disease brain is found in Arctic APP transgenic mice. Neurobiology of Aging. 30(9). 1393–1405. 75 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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