Table 2.

Cardiolipin Abnormalities in Animal Models of Aging and Neurological Disorders^a

Condition	Model/biological sample	Cardiolipin abnormalities	Refs
AD	Brain from 3xTg-AD mice (3 months old)	• Lower CL content in synaptic mitochondria • No change in CL saturation	[59]
Aging	Mouse brain cortex (3 and 17 months)	• 21% decrease of total CL in synaptic-mitochondria in 17-month- old mice	[41]
	Brain from 24-month-old rats	• 31% decrease of total CL	[42]
	Brain from 20–24-month-old rats	• 25% decrease of total CL	[40]
ALS	Motor cortex and spinal cord from asymptomatic (SOD1-G93A 70 days) and symptomatic (SOD1-G93A 120 days) ALS rats	• Reduced CL levels in the spinal cord of symptomatic rats	[52]
BTHS	Brain tissue from TAZ-KD mice	• Increased MLCL (19-fold) and decreased CL	[117]
PD	Brain tissue from Parkin-KO mice (2 and 24 months old)	• No change in total CL levels • CL remodeling defects with increase of short saturated CL acyl- chains in 24-month-old mice	[71]
	Brain and plasma from rats exposed to rotenone	• Increase of CLox in the substantia nigra • Increase of PUFA-containing CL in the plasma	[83]
TBI	Brain tissue and plasma from rats after controlled cortical impact (CCI)	• Decreased cortical CL (4 and 24 h after TBI) • Decreased CL in noncontusional areas (hippocampus and thalamus) • Increased in plasma levels of brain-specific CL (24 h after TBI)	[73,74,77]

^aAbbreviations: AD, Alzheimer’s disease; ALS, amyotrophic lateral sclerosis; BTHS, Barth syndrome; CL, cardiolipin; CLox, oxidized CL; KD, knockdown; KO, knockout; MLCL, monolysocardiolipin; PD, Parkinson’s disease; PUFA, polyunsaturated fatty acids; SOD1, superoxide dismutase 1; TBI, traumatic brain injury; TAZ, tafazzin.