Table 1.

Summary of Pin1 changes in neurodegenerative diseases

Neurodegenerative disease	Pin 1 changes observed in human samples	Pin 1 putative role	References
Alzheimer’s disease	Pin1 has been reported to be oxidatively modified, with consequent reduced activity and expression in hippocampus from MCI and AD patients compared to age-matched controls.	Protective role against age-associated neurodegeneration	[10, 11]
	Change in Pin1 neuronal localization, with a shift from nucleus to cytoplasm, have been found in postmortem human brains from AD patients compared to age-matched controls.		[12–14]
	Loss of Pin1 within the synapses of human frontal tissues from AD patients compared to age-matched control brains.		[12]
	Pin1 co-localized with deposits of aggregated tau.		[15]
Frontotemporal dementias	Overall reduction of Pin1 and redirection of the predominantly nuclear Pin1 into the neuronal cytoplasm in FTD postmortem brains compared to normal brains.	Protective role against age-associated neurodegeneration	[16]
	A trend for downregulation of Pin1 in human non-motor cortex and in the spinal cord derived from patients with FTLD-U.		[17]
Parkinson disease	Pin1 has been reported to accumulate in the Lewy Bodies of human PD brains and to co-localize with α-synuclein inclusions.	Neurotoxic action by promoting with α-synuclein inclusions	[18]
	Increased levels of Pin1 have been observed in pigmented dopaminergic neurons in postmortem human brains from PD patients.	Neurotoxic action contributing to dopaminergic neurodegeneration	[19]
Huntington disease	No data on human samples are available, but only in vitro and in vivo preclinical results.	Neurotoxic action by promoting p53-dependent neuronal apoptosis induced by mutant huntingtin	[20]
Amyotrophic lateral sclerosis	Downregulation of Pin1 expression in the spinal cord and non-motor cortex of a cohort of ALS patients.	Protective role against neurofilament-H hyperphosphorylation and its perikaryal accumulation in in vitro models	[17, 21]