PMID- 23383397
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20130206
LR  - 20220316
IS  - 2165-591X (Print)
IS  - 2165-591X (Electronic)
IS  - 2165-591X (Linking)
VI  - 1
IP  - 3
DP  - 2012
TI  - Interactions between oestrogen and the renin angiotensin system - potential 
      mechanisms for gender differences in Alzheimer's disease.
PG  - 266-79
AB  - Interactions between oestrogen and the renin angiotensin system (RAS) are 
      reviewed and explored from the perspective where these interactions may modulate 
      risk of developing Alzheimer's disease (AD). AD is more prevalent in women than 
      men, partly attributed to women's increased life expectancy; however underlying 
      vascular differences may also contribute to AD risk. The RAS is a key regulator 
      of blood pressure (BP). Pharmacological inhibition of angiotensin converting 
      enzyme (ACE) and blockade of angiotensin II type 1 receptors (AT1R) are widely 
      used to treat hypertension. Variation in components of the RAS such as ACE, 
      neprilysin (NEP) and AT1R have been reported in AD, some of which may also 
      directly alter AD neuropathology with changes in amyloid beta (Abeta) levels, 
      cognitive decline and neuroinflammation. Recently, RAS inhibiting drugs have been 
      shown to attenuate the incidence, progression and pathology of AD. Oestrogen is 
      also thought to prevent hypertension by reducing the vasoconstrictive actions of 
      the RAS. Reduced oestrogen levels in women during the menopausal transition may 
      therefore increase their risk of hypertension and/or RAS-mediated changes to 
      cerebrovascular or AD pathology. Specifically, oestrogen prevents the production 
      and action of angiotensin II (Ang II), thought to exert harmful effects of the 
      RAS in both hypertension and AD, while also potentially facilitating RAS-mediated 
      Abeta degradation. These oestrogen-RAS interactions may partly explain current 
      conflicting findings regarding oestrogen depletion and hormone therapy with 
      respect to AD risk. Clinical trials targeting either the RAS or oestrogen systems 
      for AD prevention and treatment should perhaps give closer attention to key 
      biochemical components of these pathways as potential confounders to primary and 
      secondary outcome measures.
FAU - O'Hagan, Thomas Simon
AU  - O'Hagan TS
AD  - Dementia Research Group, John James Laboratories, School of Clinical Sciences, 
      University of Bristol, Frenchay Hospital Bristol, BS16 1LE.
FAU - Wharton, Whitney
AU  - Wharton W
FAU - Kehoe, Patrick Gavin
AU  - Kehoe PG
LA  - eng
PT  - Journal Article
DEP - 20121118
PL  - United States
TA  - Am J Neurodegener Dis
JT  - American journal of neurodegenerative disease
JID - 101585753
PMC - PMC3560469
OTO - NOTNLM
OT  - Alzheimer's disease
OT  - Oestrogen
OT  - gender difference
OT  - renin angiotensin system (RAS)
EDAT- 2013/02/06 06:00
MHDA- 2013/02/06 06:01
PMCR- 2012/11/18
CRDT- 2013/02/06 06:00
PHST- 2012/10/12 00:00 [received]
PHST- 2012/11/09 00:00 [accepted]
PHST- 2013/02/06 06:00 [entrez]
PHST- 2013/02/06 06:00 [pubmed]
PHST- 2013/02/06 06:01 [medline]
PHST- 2012/11/18 00:00 [pmc-release]
PST - ppublish
SO  - Am J Neurodegener Dis. 2012;1(3):266-79. Epub 2012 Nov 18.