In propionic acidemia , a rare inherited genetic disorder, propionate acts as a metabolic toxin in liver cells by accumulating in mitochondria as propionyl-CoA and its derivative, methylcitrate, two tricarboxylic acid cycle inhibitors. Propanoate is metabolized oxidatively by glia , which suggests astrocytic vulnerability in propionic acidemia when intramitochondrial propionyl-CoA may accumulate. Propionic acidemia may alter both neuronal and glial gene expression by affecting histone acetylation.   When propionic acid is infused directly into rodents' brains, it produces reversible behavior (., hyperactivity , dystonia , social impairment, perseveration ) and brain changes (., innate neuroinflammation, glutathione depletion) that may be used as a means to model autism in rats. 
As for aldehydes , the hydrogen atoms on the carbon adjacent ("α to") the carboxyl group in esters are sufficiently acidic to undergo deprotonation, which in turn leads to a variety of useful reactions. Deprotonation requires relatively strong bases, such as alkoxides . Deprotonation gives a nucleophilic enolate , which can further react, ., the Claisen condensation and its intramolecular equivalent, the Dieckmann condensation . This conversion is exploited in the malonic ester synthesis , wherein the diester of malonic acid reacts with an electrophile (., alkyl halide ), and is subsequently decarboxylated. Another variation is the Fráter–Seebach alkylation .