The role of parvalbumin interneuron dysfunction across neurodegenerative dementias.

Autor: Smeralda CL; Precision Neuroscience & Neuromodulation Program, Gordon Center for Medical Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Siena Brain Investigation & Neuromodulation Lab (Si-BIN Lab), Unit of Neurology and Clinical Neurophysiology, Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy., Pandit S; Precision Neuroscience & Neuromodulation Program, Gordon Center for Medical Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA., Turrini S; Precision Neuroscience & Neuromodulation Program, Gordon Center for Medical Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA; Centro Studi e Ricerche in Neuroscienze Cognitive, Dipartimento di Psicologia, University of Bologna, Italy., Reilly J; Precision Neuroscience & Neuromodulation Program, Gordon Center for Medical Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA., Palmisano A; Chair of Lifespan Developmental Neuroscience, TUD Dresden University of Technology, Dresden, Germany., Sprugnoli G; Precision Neuroscience & Neuromodulation Program, Gordon Center for Medical Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA., Hampel H; Sorbonne University, Alzheimer Precision Medicine (APM), AP-HP, Pitié-Salpêtrière Hospital, Paris, France., Benussi A; Neurology Unit, Department of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy; Neurology Unit, Department of Medical, Surgical and Health Sciences, University of Trieste, Trieste, Italy., Borroni B; Neurology Unit, Department of Clinical and Experimental Sciences, University of Brescia, Brescia, Italy., Press D; Cognitive Neurology Unit, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Brookline, MA, USA., Rotenberg A; Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA., El Fakhri G; Gordon Center for Medical Imaging, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA., Koch G; Human Physiology Unit, Department of Neuroscience and Rehabilitation, University of Ferrara, Ferrara, Italy; Experimental Neuropsychophysiology Laboratory, IRCCS Santa Lucia Foundation, Rome, Italy., Rossi S; Siena Brain Investigation & Neuromodulation Lab (Si-BIN Lab), Unit of Neurology and Clinical Neurophysiology, Department of Medicine, Surgery and Neuroscience, University of Siena, Siena, Italy., Santarnecchi E; Precision Neuroscience & Neuromodulation Program, Gordon Center for Medical Imaging, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: esantarnecchi@mgh.harvard.edu.
Jazyk: angličtina
Zdroj: Ageing research reviews [Ageing Res Rev] 2024 Nov; Vol. 101, pp. 102509. Date of Electronic Publication: 2024 Sep 19.
DOI: 10.1016/j.arr.2024.102509
Abstrakt: Parvalbumin-positive (PV+) basket neurons are fast-spiking, non-adapting inhibitory interneurons whose oscillatory activity is essential for regulating cortical excitation/inhibition balance. Their dysfunction results in cortical hyperexcitability and gamma rhythm disruption, which have recently gained substantial traction as contributing factors as well as potential therapeutic targets for the treatment of Alzheimer's Disease (AD). Recent evidence indicates that PV+ cells are also impaired in Frontotemporal Dementia (FTD) and Dementia with Lewy bodies (DLB). However, no attempt has been made to integrate these findings into a coherent pathophysiological framework addressing the contribution of PV+ interneuron dysfunction to the generation of cortical hyperexcitability and gamma rhythm disruption in FTD and DLB. To fill this gap, we epitomized the most recent evidence on PV+ interneuron impairment in AD, FTD, and DLB, focusing on its contribution to the generation of cortical hyperexcitability and gamma oscillatory disruption and their interplay with misfolded protein accumulation, neuronal death, and clinical symptoms' onset. Our work deepens the current understanding concerning the role of PV+ interneuron dysfunction across neurodegenerative dementias, highlighting commonalities and differences among AD, FTD, and DLB, thus paving the way for identifying novel biomarkers and potential therapeutic targets for the treatment of these diseases.
Competing Interests: Declaration of Competing Interest ES and GK are scientific co-founders and SR is in the scientific advisory board of Sinaptica Therapeutics. ES is a scientific advisor for BottNeuro AG. HH declares no competing financial interests related to the present article. This work was initiated during his academic appointment at Sorbonne University, Paris, France, and reflects his opinion entirely and exclusively. He is an employee of Eisai Inc. The present article has been initiated and prepared as part of his academic position at Sorbonne University, Paris, France, and reflects his opinion entirely and exclusively. He served as Senior Associate Editor and currently as Reviewing Editor for the Journal Alzheimer’s & Dementia.
(Copyright © 2024. Published by Elsevier B.V.)
Databáze: MEDLINE
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