PMID- 33742772
OWN - NLM
STAT- MEDLINE
DCOM- 20220215
LR  - 20220215
IS  - 1752-8062 (Electronic)
IS  - 1752-8054 (Print)
IS  - 1752-8054 (Linking)
VI  - 14
IP  - 5
DP  - 2021 Sep
TI  - Optimizing clinical phenotyping to better delineate the complex relationship 
      between type 2 diabetes and Alzheimer's disease.
PG  - 1681-1688
LID - 10.1111/cts.13024 [doi]
AB  - Alzheimer's disease (AD) is the most common form of dementia, and its prevalence 
      is increasing rapidly. According to the Alzheimer's Association, over 5 million 
      adults in the United States over the age of 65 years currently have AD, and this 
      number is expected to exceed 13 million by 2050 in the absence of novel, 
      preventative strategies. Epidemiologic studies have implicated the presence of 
      type 2 diabetes mellitus (T2DM) specifically at midlife as a key modifiable risk 
      factor for AD, and AD may increase risk of dysglycemia and T2DM. However, data 
      have been inconsistent with regard to the magnitude of AD risk attributable to 
      T2DM, and the pathways underlying this apparent relationship remain poorly 
      understood. Elucidating the impact of T2DM on AD risk and progression requires 
      greater attention to the myriad facets of T2DM pathophysiology, its comorbid 
      conditions, and attendant treatment modalities, all of which may differentially 
      impact the relationships among T2DM, cognitive decline, and AD. This mini-review 
      will summarize the discrete facets of T2DM that may influence AD risk and 
      highlight the importance of careful clinical phenotyping in both epidemiologic 
      and interventional studies to better delineate the key pathways and mechanisms 
      linking T2DM and AD.
CI  - (c) 2021 The Authors. Clinical and Translational Science published by Wiley 
      Periodicals LLC on behalf of the American Society for Clinical Pharmacology and 
      Therapeutics.
FAU - Hanson, Angela J
AU  - Hanson AJ
AD  - Division of Gerontology and General Medicine, University of Washington School of 
      Medicine, Seattle, Washington, USA.
FAU - Rubinow, Katya B
AU  - Rubinow KB
AD  - Diabetes Institute, Division of Metabolism, Endocrinology, and Nutrition, 
      Department of Medicine, University of Washington School of Medicine, Seattle, 
      Washington, USA.
LA  - eng
GR  - R01 GM111772/GM/NIGMS NIH HHS/United States
GR  - K23 AG047978/AG/NIA NIH HHS/United States
GR  - R01 AG067563/AG/NIA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20210324
PL  - United States
TA  - Clin Transl Sci
JT  - Clinical and translational science
JID - 101474067
RN  - 0 (Blood Glucose)
SB  - IM
MH  - Alzheimer Disease/blood/*epidemiology/metabolism/physiopathology
MH  - Blood Glucose/metabolism
MH  - Blood-Brain Barrier/metabolism
MH  - Brain/metabolism/physiopathology
MH  - Diabetes Mellitus, Type 2/blood/*epidemiology/metabolism/physiopathology
MH  - Disease Progression
MH  - Humans
MH  - Prevalence
MH  - Risk Factors
PMC - PMC8504820
COIS- The authors declare no competing interests for this work.
EDAT- 2021/03/21 06:00
MHDA- 2022/02/16 06:00
PMCR- 2021/09/01
CRDT- 2021/03/20 12:14
PHST- 2021/02/25 00:00 [revised]
PHST- 2020/12/29 00:00 [received]
PHST- 2021/02/25 00:00 [accepted]
PHST- 2021/03/21 06:00 [pubmed]
PHST- 2022/02/16 06:00 [medline]
PHST- 2021/03/20 12:14 [entrez]
PHST- 2021/09/01 00:00 [pmc-release]
AID - CTS13024 [pii]
AID - 10.1111/cts.13024 [doi]
PST - ppublish
SO  - Clin Transl Sci. 2021 Sep;14(5):1681-1688. doi: 10.1111/cts.13024. Epub 2021 Mar 
      24.