Differential response of neurons to autophagy modulation in Huntington’s disease

Huntington’s disease (HD) is caused by the expansion of poly-glutamine repeats in the Huntingtin (Htt) gene and is associated with a wide variety of motor and physiological (sleep, metabolism, etc.) perturbations. Studies from diverse model organisms have proposed that modulation of autophagy (a key...

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Main Authors: Ankit Sharma, Sushma Rao, Ravi Manjithaya, Vasu Sheeba
Format: Article
Language:English
Published: Taylor & Francis Group 2025-12-01
Series:Autophagy Reports
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Online Access:https://www.tandfonline.com/doi/10.1080/27694127.2025.2519102
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author Ankit Sharma
Sushma Rao
Ravi Manjithaya
Vasu Sheeba
author_facet Ankit Sharma
Sushma Rao
Ravi Manjithaya
Vasu Sheeba
author_sort Ankit Sharma
collection DOAJ
description Huntington’s disease (HD) is caused by the expansion of poly-glutamine repeats in the Huntingtin (Htt) gene and is associated with a wide variety of motor and physiological (sleep, metabolism, etc.) perturbations. Studies from diverse model organisms have proposed that modulation of autophagy (a key protein homeostatic pathway) can mitigate the toxic effects of mutant HTT protein. However, consistent changes are not observed across studies, and the improvements in phenotypes can be associated with changes in specific circuits/neurons affected by the mutant HTT protein. They suggest that not all neurons respond effectively to autophagy modulation. Hence, it remains to be understood whether diverse circuits/neurons affected by mutant HTT protein respond effectively to this intervention. Using a genetic approach, we expressed mutant HTT protein independently in diverse sets of neurons in male Drosophila melanogaster and asked whether genetic modulation of autophagy pathway through Atg8a overexpression can mitigate the toxic effect of mutant HTT protein. We found that in male flies, not all neurons/circuits expressing mutant HTT protein respond effectively to ATG8a protein. Circadian neurons and neurons regulating carbohydrate and lipid metabolism (Dilp2+ve) showed improvement, while motor and neurons responding to temperature changes showed no improvement. Using cellular markers we also showed that these phenotypes can be attributed to specific changes in mutant HTT and Ref(2)P proteins (autophagy marker). Our study suggests that not all circuits respond effectively to autophagy modulation and suggests a potential cause for low success of autophagy modulators in clinical trials..
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spelling doaj-art-18d3825fdbaf4c8b8aaaa94daec6f9942025-08-20T03:14:53ZengTaylor & Francis GroupAutophagy Reports2769-41272025-12-014110.1080/27694127.2025.2519102Differential response of neurons to autophagy modulation in Huntington’s diseaseAnkit Sharma0Sushma Rao1Ravi Manjithaya2Vasu Sheeba3Chronobiology and Behavioural Neurogenetics Laboratory, Neuroscience Unit, Jawaharlal Nehru Centre for Advanced Scientific Research, Bangalore, IndiaChronobiology and Behavioural Neurogenetics Laboratory, Neuroscience Unit, Jawaharlal Nehru Centre for Advanced Scientific Research, Bangalore, IndiaAutophagy Laboratory, Molecular Biology and Genetics Unit, Jawaharlal Nehru Centre for Advanced Scientific Research, Bangalore, IndiaChronobiology and Behavioural Neurogenetics Laboratory, Neuroscience Unit, Jawaharlal Nehru Centre for Advanced Scientific Research, Bangalore, IndiaHuntington’s disease (HD) is caused by the expansion of poly-glutamine repeats in the Huntingtin (Htt) gene and is associated with a wide variety of motor and physiological (sleep, metabolism, etc.) perturbations. Studies from diverse model organisms have proposed that modulation of autophagy (a key protein homeostatic pathway) can mitigate the toxic effects of mutant HTT protein. However, consistent changes are not observed across studies, and the improvements in phenotypes can be associated with changes in specific circuits/neurons affected by the mutant HTT protein. They suggest that not all neurons respond effectively to autophagy modulation. Hence, it remains to be understood whether diverse circuits/neurons affected by mutant HTT protein respond effectively to this intervention. Using a genetic approach, we expressed mutant HTT protein independently in diverse sets of neurons in male Drosophila melanogaster and asked whether genetic modulation of autophagy pathway through Atg8a overexpression can mitigate the toxic effect of mutant HTT protein. We found that in male flies, not all neurons/circuits expressing mutant HTT protein respond effectively to ATG8a protein. Circadian neurons and neurons regulating carbohydrate and lipid metabolism (Dilp2+ve) showed improvement, while motor and neurons responding to temperature changes showed no improvement. Using cellular markers we also showed that these phenotypes can be attributed to specific changes in mutant HTT and Ref(2)P proteins (autophagy marker). Our study suggests that not all circuits respond effectively to autophagy modulation and suggests a potential cause for low success of autophagy modulators in clinical trials..https://www.tandfonline.com/doi/10.1080/27694127.2025.2519102Drosophila melanogasterHuntington’s diseaseautophagycircadian rhythmsleepmotor neurons
spellingShingle Ankit Sharma
Sushma Rao
Ravi Manjithaya
Vasu Sheeba
Differential response of neurons to autophagy modulation in Huntington’s disease
Autophagy Reports
Drosophila melanogaster
Huntington’s disease
autophagy
circadian rhythm
sleep
motor neurons
title Differential response of neurons to autophagy modulation in Huntington’s disease
title_full Differential response of neurons to autophagy modulation in Huntington’s disease
title_fullStr Differential response of neurons to autophagy modulation in Huntington’s disease
title_full_unstemmed Differential response of neurons to autophagy modulation in Huntington’s disease
title_short Differential response of neurons to autophagy modulation in Huntington’s disease
title_sort differential response of neurons to autophagy modulation in huntington s disease
topic Drosophila melanogaster
Huntington’s disease
autophagy
circadian rhythm
sleep
motor neurons
url https://www.tandfonline.com/doi/10.1080/27694127.2025.2519102
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AT sushmarao differentialresponseofneuronstoautophagymodulationinhuntingtonsdisease
AT ravimanjithaya differentialresponseofneuronstoautophagymodulationinhuntingtonsdisease
AT vasusheeba differentialresponseofneuronstoautophagymodulationinhuntingtonsdisease