PMID- 31333086
OWN - NLM
STAT- MEDLINE
DCOM- 20200416
LR  - 20211204
IS  - 1873-4286 (Electronic)
IS  - 1381-6128 (Linking)
VI  - 25
IP  - 23
DP  - 2019
TI  - Therapeutic Approaches to Alzheimer's Type of Dementia: A Focus on FGF21 Mediated 
      Neuroprotection.
PG  - 2555-2568
LID - 10.2174/1381612825666190716101411 [doi]
AB  - Neurodegenerative disorders are the most devastating disorder of the nervous 
      system. The pathological basis of neurodegeneration is linked with dysfunctional 
      protein trafficking, mitochondrial stress, environmental factors and aging. With 
      the identification of insulin and insulin receptors in some parts of the brain, 
      it has become evident that certain metabolic conditions associated with insulin 
      dysfunction like Type 2 diabetes mellitus (T2DM), dyslipidemia, obesity etc., are 
      also known to contribute to neurodegeneration mainly Alzheimer's Disease (AD). 
      Recently, a member of the fibroblast growth factor (FGF) superfamily, FGF21 has 
      proved tremendous efficacy in diseases like diabetes mellitus, obesity and 
      insulin resistance (IR). Increased levels of FGF21 have been reported to exert 
      multiple beneficial effects in metabolic syndrome. FGF21 receptors are present in 
      certain areas of the brain involved in learning and memory. However, despite 
      extensive research, its function as a neuroprotectant in AD remains elusive. 
      FGF21 is a circulating endocrine hormone which is mainly secreted by the liver 
      primarily in fasting conditions. FGF21 exerts its effects after binding to FGFR1 
      and co-receptor, beta-klotho (KLB). It is involved in regulating energy via glucose 
      and lipid metabolism. It is believed that aberrant FGF21 signalling might account 
      for various anomalies like neurodegeneration, cancer, metabolic dysfunction etc. 
      Hence, this review will majorly focus on FGF21 role as a neuroprotectant and 
      potential metabolic regulator. Moreover, we will also review its potential as an 
      emerging candidate for combating metabolic stress induced neurodegenerative 
      abnormalities.
CI  - Copyright(c) Bentham Science Publishers; For any queries, please email at 
      epub@benthamscience.net.
FAU - Taliyan, Rajeev
AU  - Taliyan R
AD  - Department of Pharmacy, Birla Institute of Technology and Science, Pilani-333031, 
      Rajasthan, India.
FAU - Chandran, Sarathlal K
AU  - Chandran SK
AD  - Department of Pharmacy, Birla Institute of Technology and Science, Pilani-333031, 
      Rajasthan, India.
FAU - Kakoty, Violina
AU  - Kakoty V
AD  - Department of Pharmacy, Birla Institute of Technology and Science, Pilani-333031, 
      Rajasthan, India.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United Arab Emirates
TA  - Curr Pharm Des
JT  - Current pharmaceutical design
JID - 9602487
RN  - 0 (KLB protein, human)
RN  - 0 (Membrane Proteins)
RN  - 0 (fibroblast growth factor 21)
RN  - 62031-54-3 (Fibroblast Growth Factors)
RN  - EC 2.7.10.1 (FGFR1 protein, human)
RN  - EC 2.7.10.1 (Receptor, Fibroblast Growth Factor, Type 1)
RN  - EC 3.2.1.31 (Klotho Proteins)
SB  - IM
MH  - Alzheimer Disease/*therapy
MH  - Fibroblast Growth Factors/*physiology
MH  - Humans
MH  - Klotho Proteins
MH  - Membrane Proteins/physiology
MH  - *Neuroprotection
MH  - Receptor, Fibroblast Growth Factor, Type 1/physiology
OTO - NOTNLM
OT  - Alzheimer's disease
OT  - Metabolic syndrome
OT  - diabetes mellitus
OT  - fibroblast growth factor 21
OT  - insulin resistance
OT  - neurodegeneration.
EDAT- 2019/07/25 06:00
MHDA- 2020/04/17 06:00
CRDT- 2019/07/24 06:00
PHST- 2019/06/19 00:00 [received]
PHST- 2019/07/08 00:00 [accepted]
PHST- 2019/07/25 06:00 [pubmed]
PHST- 2020/04/17 06:00 [medline]
PHST- 2019/07/24 06:00 [entrez]
AID - CPD-EPUB-99645 [pii]
AID - 10.2174/1381612825666190716101411 [doi]
PST - ppublish
SO  - Curr Pharm Des. 2019;25(23):2555-2568. doi: 10.2174/1381612825666190716101411.