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Ultrasonic repression of TRPA1-dependent astrocyte reactivity confers neuroprotection in models of Lewy body dementia

Ji Hun Kim, Keunhyung Lee, Minseok Koo, Doeun Kim, Jin Kyung Hong, Jeong-Yun Choi, Han Seok Ko, Joo-Ho Shin, Joo Min Park, Jinhyoung Park, Yunjong Lee

Translational Neurodegeneration 2026, 15 · 10.1186/s40035-026-00544-6

rodentin vitro cellothercellular imaginghistology molecularbehaviour

Abstract

Background The pathology of Lewy body dementia (LBD) features neuronal α-synuclein (α-syn) accumulation and astrocytic hyperactivation in cognitive brain circuits. Ultra-low-intensity ultrasound (ULIUS) modulates astrocyte function via transient receptor potential ankyrin 1 (TRPA1) and has been investigated for therapeutic applications in neurodegenerative diseases. Methods The therapeutic efficacy and mechanisms of ULIUS were evaluated in primary cultured astrocytes and neuron-glia cocultures treated with α-syn preformed fibrils (PFFs), as well as in an LBD model induced by hippocampal α-syn PFF injection into neuronal α-syn-A53T transgenic mice. Astrocytic TRPA1 was modulated under pathologic conditions with ULIUS or a pharmacologic TRPA1 antagonist to determine calcium responses and transcriptional regulation of Trpa1 and inflammation-related genes. Neuropathological analyses for Lewy-like inclusions, neurodegeneration, and inflammation were performed in LBD mouse brains, with or without ULIUS. Spatial learning and memory were assessed using the Barnes maze. Results Repeated transcranial ULIUS application was safe in long-term use and, unlike prolonged stronger ultrasound, did not cause hippocampal inflammation or neurodegeneration. It also prevented neuroinflammation and Lewy-like pathologies, rescuing cognitive impairment in LBD mice. ULIUS abolished α-syn-induced elevation of TRPA1, toll-like receptors-2 (TLR2), interleukin-1β, and tumor necrosis factor-α in LBD mouse brains. Mechanistically, both ULIUS and TRPA1 inhibitor blocked the sustained TRPA1-dependent calcium increase and the expression of inflammation-associated transcripts in α-syn PFF-treated astrocytes. Conclusions Our findings provide mechanistic insights into the reciprocal TRPA1-TLR2 signaling pathway in α-syn-induced astrocyte pathology and underscore the disease-modifying potential of focused transcranial ULIUSm on astrocytes for the treatment of LBD. This study establishes a novel therapeutic strategy to alleviate neuroinflammation and cognitive decline associated with LBD. The demonstration of its long-term safety further supports ULIUS as a promising therapeutic strategy.

Abstract via europepmc.

Speciesmouse (C57BL/6J wild-type; α-syn A53T transgenic)
Subjects10 animals
Sessions per subject10
Randomisednot reported
Blindingnot reported
Sham / controlnone
Auditory controlnot reported
Readout timingboth
Anaesthesiaanaesthetised
Readoutscellular imaging, histology molecular, behaviourFluo-4AM calcium imaging; RT-qPCR (Trpa1, Tlr2, Tlr4, Tnf-alpha, Il-1beta, Il-1r1, Gfap); western blot (alpha-synuclein, TRPA1, TLR2); immunohistochemistry/immunofluorescence (pS129-alpha-synuclein, GFAP, Iba-1, tyrosine hydroxylase); Barnes maze, Y-maze, pole test, rotarod
Direction of effectinhibitoryUltrasound suppressed alpha-syn PFF-induced TRPA1 and TLR2 upregulation, sustained astrocytic calcium influx, and pro-inflammatory cytokine expression in vitro; transcranially, it reduced neuroinflammation (astrogliosis, microgliosis), Lewy-like pathology and hippocampal neurodegeneration, and rescued cognitive impairment in the LBD mouse model.
Adverse eventsobservedRepeated transcranial ULIUS at 0.2 W/cm2 for one month produced no detectable pathological changes in wild-type mice, whereas a stronger paradigm (2.5 W/cm2, same 10-session schedule) caused reduced dentate gyrus thickness, hippocampal neuron loss, and increased microgliosis/astrogliosis, indicating an intensity-dependent safety margin.

Exposures

Exposure 1: In vitro ultrasound stimulation of primary cortical neuron-glia co-culture and primary astrocyte culture (Ultrasonocoverslip)

Target: cultured neurons, cultured glia — “primary cortical neuron-glia co-culture and primary astrocyte culture on Ultrasonocoverslip
Device: custom-built · Ultrasonocoverslip (PVDF-TrFE piezoelectric transducer integrated with glass coverslip)

Pulse timing
Waveformpulsed
Fundamental frequency (kHz)6,000✓✓
Pulse duration (ms)0.333✓✓
Pulse repetition frequency (Hz)1,500✓✓
Duty cycle (%)50pulse duration × PRF gives 49.95%✓✓
Sonication duration (s)0.5✓✓
Pressure and intensity, by domain
Free-field pressure (kPa)110✓✓
Free-field Isppa (W/cm²)not reported
Free-field Ispta (W/cm²)0.2✓✓
In-situ estimatenot applicable
In-situ pressure (kPa)not applicable
In-situ Isppa (W/cm²)not applicable
In-situ Ispta (W/cm²)not applicable
Protocol, in the paper’s words

Cells received three trials of ultrasound stimulation with 2-min intervals in a single day; this session was repeated every 2 days for three sessions total (astrocyte cultures) or every other day for three sessions (neuron-glia co-culture).

Exposure 2: Transcranial ultrasound stimulation of hippocampus (dentate gyrus) in vivo

Target: dentate gyrus — “hippocampus (dentate gyrus, α-syn PFF injection site)
Device: custom-built · custom-made 1 MHz focused single-element transducer, focal distance 3 mm

Pulse timing
Waveformpulsed
Fundamental frequency (kHz)1,000✓✓
Pulse duration (ms)0.333✓✓
Pulse repetition frequency (Hz)1,500✓✓
Duty cycle (%)50pulse duration × PRF gives 49.95%✓✓
Sonication duration (s)0.5✓✓
Pressure and intensity, by domain
Free-field pressure (kPa)not reported
Free-field Isppa (W/cm²)not reported
Free-field Ispta (W/cm²)not reported
In-situ estimatemeasurementsingle value
In-situ pressure (kPa)110✓✓
In-situ Isppa (W/cm²)not reported
In-situ Ispta (W/cm²)not reported
Ispta, domain unspecified (W/cm²)0.2✓✓
Protocol, in the paper’s words

Ultrasound was delivered to the injected hippocampal region across the intact skull three times per day with 2-min intervals; this session was repeated every 3 days for 1 month, for a total of 10 sessions, under 1% isoflurane anaesthesia. A separate safety comparison in wild-type mice used a stronger paradigm (2.5 W/cm2, 10 sessions over one month) alongside the main 0.2 W/cm2 paradigm.

Flags from extraction

  • exposures[0].fundamental_frequency_khzMethods state the stimulation used '333-μs-long 6-MHz bursts', but the Results section separately states 'the operational frequency of the transducer was 6.1 MHz'; recorded as 6 MHz (6000 kHz) per the stimulation-protocol sentence, minor discrepancy with the 6.1 MHz figure-caption value.
  • n_subjectsMultiple cohorts (wild-type safety mice, alpha-syn transgenic LBD mice, littermate controls) and multiple assays with different per-group n (e.g. n=10 for Barnes maze, n=5 for immunohistochemistry, n=3 for western blot) are reported; no single total number of ultrasound-exposed animals is stated.
  • exposures[1].unspecified_domain.isppa_w_cm20.2 W/cm2 is the main therapeutic ISPTA used throughout; 2.5 W/cm2 is a separate higher-intensity paradigm tested only for safety comparison in wild-type mice, not used in the LBD therapeutic experiments; domain (pre- vs post-cranial) not stated for either intensity value.
  • exposures[0].target.termsIn vitro experiments used both a neuron-glia-microglia co-culture and a purified primary astrocyte culture under the same ultrasound protocol; both target terms are listed for this single exposure.
  • exposures[0].in_situIn vitro exposure is a cell-culture dish with no skull/tissue path; in_situ fields would ideally be null, but the paper's overall model_system also includes an in-vivo rodent exposure, so in_situ is recorded as not_reported rather than a value.