PMID- 34489627
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20210908
IS  - 1662-4548 (Print)
IS  - 1662-453X (Electronic)
IS  - 1662-453X (Linking)
VI  - 15
DP  - 2021
TI  - Role of DPP-4 and SGLT2 Inhibitors Connected to Alzheimer Disease in Type 2 
      Diabetes Mellitus.
PG  - 708547
LID - 10.3389/fnins.2021.708547 [doi]
LID - 708547
AB  - Alzheimer's disease (AD) is characterized by memory loss and cognitive decline. 
      Additionally, abnormal extracellular amyloid plaques accumulation and nerve 
      damage caused by intracellular neurofibrillary tangles, and tau protein are 
      characteristic of AD. Furthermore, AD is associated with oxidative stress, 
      impaired mitochondrial structure and function, denormalization, and inflammatory 
      responses. Recently, besides the amyloid beta hypothesis, another hypothesis linking 
      AD to systemic diseases has been put forth by multiple studies as a probable 
      cause for AD. Particularly, type 2 diabetes mellitus (T2DM) and its features, 
      including hyperinsulinemia, and chronic hyperglycemia with an inflammatory 
      response, have been shown to be closely related to AD through insulin resistance. 
      The brain cannot synthesize or store glucose, but it does require glucose, and 
      the use of glucose in the brain is higher than that in any other organ in the 
      mammalian body. One of the therapeutic drugs for T2DM, dipeptidyl peptidase-4 
      (DPP-4) inhibitor, suppresses the degradation of incretins, glucagon-like 
      peptides and glucose-dependent insulinotropic peptide. Sodium-glucose 
      cotransporter 2 (SGLT2) inhibitors, recently used in T2DM treatment, have a 
      unique mechanism of action via inhibition of renal glucose reabsorption, and 
      which is different from the mechanisms of previously used medications. This 
      manuscript reviews the pathophysiological relationship between the two diseases, 
      AD and T2DM, and the pharmacological effects of therapeutic T2DM drugs, 
      especially DPP-4 inhibitors, and SGLT2 inhibitors.
CI  - Copyright (c) 2021 Sim, Barua, Kim, Lee and Lee.
FAU - Sim, A Young
AU  - Sim AY
AD  - Department of Anatomy, Yonsei University College of Medicine, Seoul, South Korea.
AD  - Brain Korea 21 Plus Project for Medical Science, Yonsei University College of 
      Medicine, Seoul, South Korea.
FAU - Barua, Sumit
AU  - Barua S
AD  - Department of Anatomy, Yonsei University College of Medicine, Seoul, South Korea.
FAU - Kim, Jong Youl
AU  - Kim JY
AD  - Department of Anatomy, Yonsei University College of Medicine, Seoul, South Korea.
FAU - Lee, Yong-Ho
AU  - Lee YH
AD  - Department of Internal Medicine, Yonsei University College of Medicine, Seoul, 
      South Korea.
FAU - Lee, Jong Eun
AU  - Lee JE
AD  - Department of Anatomy, Yonsei University College of Medicine, Seoul, South Korea.
AD  - Brain Korea 21 Plus Project for Medical Science, Yonsei University College of 
      Medicine, Seoul, South Korea.
AD  - Brain Research Institute, Yonsei University College of Medicine, Seoul, South 
      Korea.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20210811
PL  - Switzerland
TA  - Front Neurosci
JT  - Frontiers in neuroscience
JID - 101478481
PMC - PMC8417940
OTO - NOTNLM
OT  - Alzheimer's disease
OT  - DPP-4 inhibitor
OT  - SGLT2 inhibitor
OT  - insulin resistance
OT  - insulin signaling
OT  - type 2 diabetes mellitus
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2021/09/08 06:00
MHDA- 2021/09/08 06:01
PMCR- 2021/01/01
CRDT- 2021/09/07 07:41
PHST- 2021/05/12 00:00 [received]
PHST- 2021/07/12 00:00 [accepted]
PHST- 2021/09/07 07:41 [entrez]
PHST- 2021/09/08 06:00 [pubmed]
PHST- 2021/09/08 06:01 [medline]
PHST- 2021/01/01 00:00 [pmc-release]
AID - 10.3389/fnins.2021.708547 [doi]
PST - epublish
SO  - Front Neurosci. 2021 Aug 11;15:708547. doi: 10.3389/fnins.2021.708547. 
      eCollection 2021.