Vol.:(0123456789) 1 3
Neurochemical Research
https://doi.org/10.1007/s11064-020-02993-5
REVIEW
The Novel Role of PPAR Alpha in the Brain: Promising Target in Therapy
of Alzheimer’s Disease and Other Neurodegenerative Disorders
Sylwia Wójtowicz
1
· Anna K. Strosznajder
2
· Mieszko Jeżyna
2
· Joanna B. Strosznajder
1
Received: 8 December 2019 / Revised: 11 February 2020 / Accepted: 17 February 2020
© The Author(s) 2020
Abstract
Peroxisome proliferator activated receptor alpha (PPAR-α) belongs to the family of ligand-regulated nuclear receptors
(PPARs). These receptors after heterodimerization with retinoid X receptor (RXR) bind in promotor of target genes to PPAR
response elements (PPREs) and act as a potent transcription factors. PPAR-α and other receptors from this family, such as
PPAR-β/δ and PPAR-γ are expressed in the brain and other organs and play a signifcant role in oxidative stress, energy
homeostasis, mitochondrial fatty acids metabolism and infammation. PPAR-α takes part in regulation of genes coding pro-
teins that are involved in glutamate homeostasis and cholinergic/dopaminergic signaling in the brain. Moreover, PPAR-α
regulates expression of genes coding enzymes engaged in amyloid precursor protein (APP) metabolism. It activates gene
coding of α secretase, which is responsible for non-amyloidogenic pathway of APP degradation. It also down regulates β
secretase (BACE-1), the main enzyme responsible for amyloid beta (Aβ) peptide release in Alzheimer Diseases (AD). In
AD brain expression of genes of PPAR-α and PPAR-γ coactivator-1 alpha (PGC-1α) is signifcantly decreased. PPARs are
altered not only in AD but in other neurodegenerative/neurodevelopmental and psychiatric disorder. PPAR-α downregula-
tion may decrease anti-oxidative and anti-infammatory processes and could be responsible for the alteration of fatty acid
transport, lipid metabolism and disturbances of mitochondria function in the brain of AD patients. Specifc activators of
PPAR-α may be important for improvement of brain cells metabolism and cognitive function in neurodegenerative and
neurodevelopmental disorders.
Keywords PPAR-α · Glutamatergic signaling · App/aβ metabolism · Mitochondria function · Neurodegeneration ·
Neuroprotection
Introduction
Peroxisome proliferators activated receptors (PPARs) are
family of ligand-regulated nuclear receptors that include
PPAR-α, PPAR-β/δ and PPAR-γ. These receptors are
encoded by distinct genes: PPAR-α (NR1C1), PPAR-β/δ
(NUC1 or NR1C2) and PPAR-γ (NR1C3) located on chro-
mosome 15, 17, and 6 in the mouse and on chromosome 22,
6, 3 in humans. The PPAR-γ gene alternative promotors are
responsible for three isoforms (γ1, γ2, γ3) These PPARs
genes encode proteins of 468, 441, 475 and 505 amino acids
with 49–56 kDa [1, 2].
PPARs regulate transcriptions through a complex mecha-
nism as described in review by Berger and Moller [3] and
Nierenberg et al. [4]. The frst PPAR currently known as
PPAR-α was discovered in 1990 [5]. PPARs after hetero-
dimerization with RXR bind to the specifc promotor region
of target genes described as PPAR response elements
(PPREs) and act as transcription factor(s) [4]. PPARs coacti-
vators, such as PPAR-γ coactivator-1 alpha (PGC1-α), exert
signifcant role in transcription of genes through interaction
not only with PPARs but also with other nuclear receptors
as estrogen receptors (ERs) and nuclear respiratory factors
1 and 2 (NRF1, NRF2) [6]. These receptors play a signif-
cant role in the regulation of transcription, energy and lipid
metabolism and also in thermogenesis. PPAR-α regulates
* Sylwia Wójtowicz
swojtowicz@imdik.pan.pl
* Joanna B. Strosznajder
jstrosznajder@imdik.pan.pl
1
Department of Cellular Signaling, Mossakowski Medical
Research Centre Polish Academy of Sciences, 5 Pawińskiego
st., 02-106 Warsaw, Poland
2
Faculty of Medicine, Medical University of Bialystok, 1
Kilinskiego st., 15-089 Białystok, Poland