Alban Latremoliere, MSC, PhD
Highlights
Languages
- English
Gender
MaleJohns Hopkins Affiliations:
- Johns Hopkins School of Medicine Faculty
About Alban Latremoliere
Primary Academic Title
Assistant Professor of Neurological Surgery
Background
Alban Latremoliere is an Assistant Professor in the department of Neurosurgery at Johns Hopkins University (MD, USA). He graduated in Neuroscience from the University Pierre and Marie Curie (Paris, France) and performed his postdoctoral training at the F.M. Kirby Neurobiology Center at Boston Children’s Hospital and Harvard Medical School (MA, USA). Dr. Latremoliere’s laboratory focuses on the neurobiology of sensory systems, with an emphasis on pain and regeneration. The main areas of research are: 1) Assess ongoing pain in rodent models of neuropathic pain in vivo and determine the mechanisms responsible, 2) Understand the relationship between reinnervation of target tissue after peripheral nerve regeneration and functional recovery/pain sensitivity and 3) Determine how acute and chronic pain alter sleep architecture.
Recent News Articles and Media Coverage
A Good Night's Sleep or a Cup of Coffee Makes Things Less Painful, Technology Networks (June 02, 2017)
To improve chronic pain, get more sleep (coffee helps too), Medicalxpress (May 8, 2017)
Before You Take Ibuprofen, Try This, Time (May 18, 2017)
Tracking sleep disruptions could improve nerve pain treatments NewScientist (May 2022)
Targeting Sepiapterin Reductase to Treat Neuropathic Pain, (June 22, 2015)
Additional Academic Titles
Assistant Professor of Neuroscience
Research Interests
Functional recovery, Nerve regeneration, Neural plasticity, Pain, Sleep, Translational Medicine
Lab Website
Latremoliere Lab - Lab Website
The Latremoliere lab studies the neural plasticity caused by peripheral nerve injury in mice, with an emphasis on pain and recovery of functional recovery.
Research Summary
Peripheral nerve injury can lead to neuropathic pain, a condition characterized by abnormal pain symptoms like hyperalgesia (more pain to noxious stimuli), allodynia (pain in response to innocuous stimuli) and spontaneous pain (pain in absence of external stimuli). The majority of treatments available are ineffective and display many side effects and most attempts to develop new analgesics have failed. There is, therefore a critical need to identify novel targets to develop new therapeutic approaches.
Our laboratory is studying the neural plasticity responsible for neuropathic pain using mouse genetics and behavioral/physiological approaches. Our goal is to find relevant ways to measure abnormal pain symptoms in rodent models of chronic pain and understand the underlying mechanisms to develop new treatments with improved translational efficacy.
One such pathway is the tetrahydrobiopterin (BH4) production pathway, whose role in neuropathic pain was identified through Human genetic studies. Using different tissue-specific inducible transgenic mouse lines to visualize and modulate the cells engaging the BH4 production pathway, we showed that modulating this pathway could be a viable therapeutic strategy. We are now testing the efficacy of new compounds that safely modulate BH4 production on pain hypersensitivity and other nerve injured-induced changes.
Another major complaint reported by many neuropathic pain patients is poor sleep quality, which leads to constant fatigue and lack of restorative sleep. The exact nature of the sleep disturbances caused by chronic pain is unknown, and yet this represents a critical aspect of neuropathic pain. In collaboration with Dr. Chloe Alexandre we work to characterize these sleep disturbances in mouse models of chronic pain and determine the neural networks responsible using various transgenic tools to visualize, activate or inhibit specific neurons.
Selected Publications
- Alexandre C, Miracca G, Holanda VD, Sharma A, Kourbanova K, Ferreira A, Bicca MA, Zeng X, Nassar VA, Lee S, Kaur S, Sarma SV, Sacré P, Scammell TE, Woolf CJ, Latremoliere A. (2024) Nociceptor spontaneous activity is responsible for fragmenting non-rapid eye movement sleep in mouse models of neuropathic pain. Sci Transl Med. 2024 Apr 17;16(743)
- Latremoliere A., Latini, A., Andrews, N., Cronin, S.J., Fujita, M., Gorska, K., Hovius, R., Romero, C., Chuaiphichai, S., Painter, M., Miracca, G., Babaniyi, O., Remor, A.P., Duong, K., Riva, P., Barrett, L.B., Ferreiros, N., Naylor, A., Penninger, J.M., Tegeder, I., Zhong, J., Blagg, J., Channon, K.M., Johnsson, K., Costigan, M., and Woolf, C.J. (2015). Reduction of Neuropathic and Inflammatory Pain through Inhibition of the Tetrahydrobiopterin Pathway. Neuron 86, 1393-1406
- Alexandre, C*, Latremoliere A*, Ferreira, A, Miracca, G, Yamamoto, M, Scammell, TE, and Woolf, CJ (2017). Decreased alertness due to sleep loss increases pain sensitivity in mice. Nat Med 23, 768-774
- Kourbanova, K., Alexandre, C., Latremoliere A. (2022). Effect of sleep loss on pain-New conceptual and mechanistic avenues. Front Neurosci. 16:1009902
- Liu Y*, Latremoliere A*, Li X*, Zhang Z*, Chen M, Wang X, Fang C, Zhu J, Alexandre C, Gao Z, Chen B, Ding X, Zhou JY, Zhang Y, Chen C, Wang KH, Woolf CJ, He Z. (2018). Touch and tactile neuropathic pain sensitivity are set by corticospinal projections. Nature. 2018 Sep;561(7724):547-550
Additional Training
- Postdoctoral training, Harvard Medical School & Massachusetts General Hospital - Boston, MA (2010)
- Postdoctoral training, Harvard Medical School & Boston Children’s Hospital - Boston, MA (2017)