Do SCFAs directly modulate α-synuclein aggregation in vivo at physiologically relevant brain concentrations?

Analysis ID: SDA-2026-04-12-gap-debate-20260410-113021-6fbc6da4 | Domain: neurodegeneration | Status: completed | Created: 2026-04-12T20:44:16.010329

Top Hypotheses (2 total)

#1 HDAC6 Activation as SCFA-Mediated Neuroprotective Mechanism

0.537

HDAC6, HSP90AA1

# HDAC6 Activation as SCFA-Mediated Neuroprotective Mechanism ## Enhancing Hsp90 K489 Deacetylation Through Selective HDAC6 Activation to Promote Chaperone-Mediated Autophagy of α-Synuclein Oligome

#2 Dissociating SCFA's Dual Signaling Through GPR43/GPR41 Biased Agonism

0.525

FFAR2, FFAR3, NLRP3

# Engineering GPR41-Biased SCFA Analogs to Bypass GPR43-NLRP3 Pro-Aggregation Signaling ## Mechanism of Action Short-chain fatty acids (SCFAs), principally acetate (C2), propionate (C3), and butyr

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