PMID- 26157520
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20150709
LR  - 20201001
IS  - 1874-205X (Print)
IS  - 1874-205X (Electronic)
IS  - 1874-205X (Linking)
VI  - 9
DP  - 2015
TI  - Homocysteine Induced Cerebrovascular Dysfunction: A Link to Alzheimer's Disease 
      Etiology.
PG  - 9-14
LID - 10.2174/1874205X01509010009 [doi]
AB  - A high serum level of homocysteine, known as hyperhomocystenemia (HHcy) is 
      associated with vascular dysfunction such as altered angiogenesis and increased 
      membrane permeability. Epidemiological studies have found associations between 
      HHcy and Alzheimer's disease (AD) progression that eventually leads to vascular 
      dementia (VaD). VaD is the second most common cause of dementia in people older 
      than 65, the first being AD. VaD affects the quality of life for those suffering 
      by drastically decreasing their cognitive function. VaD, a cerebrovascular 
      disease, generally occurs due to cerebral ischemic events from either decreased 
      perfusion or hemorrhagic lesions. HHcy is associated with the hallmarks of 
      dementia such as tau phosphorylation, Abeta aggregation, neurofibrillary tangle 
      (NFT) formation, neuroinflammation, and neurodegeneration. Previous reports also 
      suggest HHcy may promote AD like pathology by more than one mechanism, including 
      cerebral microangiopathy, endothelial dysfunction, oxidative stress, 
      neurotoxicity and apoptosis. Despite the corelations presented above, the 
      question still exists - does homocysteine have a causal connection to AD? In this 
      review, we highlight the role of HHcy in relation to AD by discussing its 
      neurovascular effects and amelioration with dietary supplements. Moreover, we 
      consider the studies using animal models to unravel the connection of Hcy to AD.
FAU - Kamat, P K
AU  - Kamat PK
AD  - Department of Physiology and Biophysics, School of Medicine, University of 
      Louisville, and Louisville, KY 40202, USA.
FAU - Vacek, J C
AU  - Vacek JC
AD  - Department of Physiology and Biophysics, School of Medicine, University of 
      Louisville, and Louisville, KY 40202, USA.
FAU - Kalani, A
AU  - Kalani A
AD  - Department of Physiology and Biophysics, School of Medicine, University of 
      Louisville, and Louisville, KY 40202, USA.
FAU - Tyagi, N
AU  - Tyagi N
AD  - Department of Physiology and Biophysics, School of Medicine, University of 
      Louisville, and Louisville, KY 40202, USA.
LA  - eng
GR  - R01 HL107640/HL/NHLBI NIH HHS/United States
PT  - Journal Article
DEP - 20150624
PL  - United Arab Emirates
TA  - Open Neurol J
JT  - The open neurology journal
JID - 101480493
PMC - PMC4485324
OTO - NOTNLM
OT  - Alzheimer's disease
OT  - blood brain barrier
OT  - cerebrovascular pathology
OT  - homocysteine
OT  - vascular dementia
EDAT- 2015/07/15 06:00
MHDA- 2015/07/15 06:01
PMCR- 2015/01/01
CRDT- 2015/07/10 06:00
PHST- 2014/09/29 00:00 [received]
PHST- 2014/12/01 00:00 [revised]
PHST- 2014/12/11 00:00 [accepted]
PHST- 2015/07/10 06:00 [entrez]
PHST- 2015/07/15 06:00 [pubmed]
PHST- 2015/07/15 06:01 [medline]
PHST- 2015/01/01 00:00 [pmc-release]
AID - TONEUJ-9-9 [pii]
AID - 10.2174/1874205X01509010009 [doi]
PST - epublish
SO  - Open Neurol J. 2015 Jun 24;9:9-14. doi: 10.2174/1874205X01509010009. eCollection 
      2015.