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000285456 1001_ $$0P:(DE-2719)9001282$$aScekic-Zahirovic, Jelena$$b0$$eFirst author$$udzne
000285456 245__ $$aLarge-scale mapping of the MCH network in ALS mice reveals the vulnerability of dopaminergic and GABAergic neurons in zona incerta
000285456 260__ $$aLondon$$bBiomed Central$$c2026
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000285456 520__ $$aWeight loss and hypermetabolism are early and prognostically significant features of amyotrophic lateral sclerosis (ALS) and are associated with hypothalamic atrophy and degeneration of melanin-concentrating hormone (MCH) neurons that regulate energy balance. To investigate whether MCH vulnerability arises from upstream network dysfunction, we performed whole-brain retrograde rabies tracing in SOD1G93A mice. We identified an early, selective loss of monosynaptic inputs from the zona incerta (ZI), a dopaminergic (DA)/gamma-aminobutyric acid (GABA)ergic nucleus that preceded MCH neuron degeneration. Neurochemical profiling confirmed the DA/GABAergic identity of these ZI input neurons, and ZI/DAergic neurons later degenerated. ALS-related pathology emerged early in the ZI, paralleling pathology in the motor cortex, while anterograde mapping revealed that motor cortical projections preferentially targeted the ZI, linking vulnerable motor and metabolic networks. Loss of ZI/DAergic neurons was observed in conjunction with weight loss in non-SOD1 ALS models. These findings identify the ZI as an early-affected node within hypothalamic networks and suggest that disruption of DA/GABAergic inputs to MCH neurons is associated with subsequent MCH and DA neuronal vulnerability, degeneration and metabolic imbalance in ALS.The online version contains supplementary material available at 10.1186/s40478-026-02231-z.
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000285456 650_7 $$2Other$$aAmyotrophic lateral sclerosis
000285456 650_7 $$2Other$$aDopaminergic neurons
000285456 650_7 $$2Other$$aMelanin-concentrating hormone neurons
000285456 650_7 $$2Other$$aMonosynaptic rabies tracing
000285456 650_7 $$2Other$$aWeight loss
000285456 650_7 $$2Other$$aZona incerta
000285456 7001_ $$aAntonucci, Stefano$$b1
000285456 7001_ $$0P:(DE-2719)2812844$$aWiesner, Diana$$b2$$udzne
000285456 7001_ $$aEbner, Chiara$$b3
000285456 7001_ $$aEl Hajj, Hussein$$b4
000285456 7001_ $$aAousji, Oumayma$$b5
000285456 7001_ $$0P:(DE-2719)9001676$$aHalablab, Kareen$$b6$$udzne
000285456 7001_ $$aFan, Yiting$$b7
000285456 7001_ $$aZelaya, Anneka$$b8
000285456 7001_ $$0P:(DE-2719)9001770$$aYartas, Gizem$$b9$$udzne
000285456 7001_ $$aBaskar, Karthik$$b10
000285456 7001_ $$aÇakmak, E. Anastasia$$b11
000285456 7001_ $$0P:(DE-HGF)0$$aBayer, David$$b12
000285456 7001_ $$aSung, Hoon-Ki$$b13
000285456 7001_ $$aDupuis, Luc$$b14
000285456 7001_ $$aPark, Jeehye$$b15
000285456 7001_ $$0P:(DE-2719)2812851$$aRoselli, Francesco$$b16$$eLast author$$udzne
000285456 773__ $$0PERI:(DE-600)2715589-4$$a10.1186/s40478-026-02231-z$$gVol. 14, no. 1, p. 46$$n1$$p46$$tActa Neuropathologica Communications$$v14$$x2051-5960$$y2026
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