This article by Dr. Fabricio Ferreira de Oliveira et al. is published in Current Alzheimer Research, Volume 15, Issue 4, 2018
The angiotensin-converting enzyme is an amyloid-ß-degrading enzyme. While angiotensin-converting enzyme inhibitors could increase amyloid-ß accumulation, they might also slow cognitive decline by way of cholinergic effects, by increasing brain substance P and boosting the activity of neprilysin, and by modulating glucose homeostasis and augmenting the secretion of adipokines to enhance insulin sensitivity in patients with Alzheimer’s disease dementia. In this study from São Paulo, Brazil, we aimed to investigate whether ACE polymorphisms rs1800764 and rs4291 are associated with cognitive and functional change in patients with Alzheimer’s disease dementia, while also taking APOE haplotypes and anti-hypertensive treatment with angiotensin-converting enzyme inhibitors into account for stratification. Overall, 193 consecutive patients with late-onset Alzheimer’s disease dementia were screened with cognitive tests, while their caregivers were queried for functional and caregiver burden scores. Prospective pharmacogenetic correlations were estimated for one year, considering APOE and ACE genotypes and haplotypes, and treatment with angiotensin-converting enzyme inhibitors. Almost 94% of all patients used cholinesterase inhibitors, whereas 155 had arterial hypertension, and 124 used angiotensin-converting enzyme inhibitors. No functional impacts were found regarding any genotypes or pharmacological treatment. Either for carriers of ACE haplotypes that included rs1800764 — T and rs4291 — A, or for APOE4- carriers of rs1800764 — T or rs4291 — T, angiotensin-converting enzyme inhibitors slowed cognitive decline independently of blood pressure variations, possibly by way of central and peripheral effects. APOE4+ carriers were not responsive to treatment with angiotensin-converting enzyme inhibitors. In conclusion, angiotensin-converting enzyme inhibitors may slow cognitive decline for patients with Alzheimer’s disease dementia, more remarkably for APOE4- carriers of specific ACE genotypes. Future trials should prospectively compare angiotensin-converting enzyme inhibitors according to their brain-penetrating properties since the start of anti-hypertensive therapy, with measurements of cerebrospinal fluid and serum levels and activity of the angiotensin-converting enzyme, as well as genetic profiles and neuroimaging parameters.
For more information on this research, please visit: http://www.eurekaselect.com/156397/article
Bentham Science observes World Glaucoma Week from 8th to 15th March, 2018, with the world and presents full support for the victims of glaucoma through publishing the latest research developments to combat this dangerous eye disease. Glaucoma is a widely feared eye problem because it causes irreversible blindness. Eye researchers and ophthalmologists have mostly attributed glaucoma to the increase in intraocular pressure, i.e. the increase in fluid pressure inside the eye.
However there are cases where the glaucoma patients had normal intraocular pressure, which suggests that there are other factors that can cause or enhance the risk of contracting this disease. Researchers from the Ophthalmology Unit of the University of Rome Tor Vergata have recently discovered that the patients of Alzheimer’s were often found susceptible of getting glaucoma in their eyes. Alzheimer’s disease is the most common form of dementia in the elderly that hampers memory and understanding.
Both these neurodegenerative diseases were found to have very similar risk factors and often co-existed in the older people. The research is an important revelation and opens doors for future studies and possible progress in finding cure for both Alzheimer’s disease and glaucoma.
The research entitled, Glaucoma and Alzheimer Disease: One Age-Related Neurodegenerative Disease of the Brain, is published in the Bentham Science journal, Current Neuropharmacology.
Article by Disease on “Neuroscience”
The blood-brain barrier (BBB) is a physiological regulator of transport of essential items from blood to brain for the maintenance of homeostasis of the central nervous system (CNS) within narrow limits. The BBB is also responsible for export of harmful or metabolic products from brain to blood to keep the CNS fluid microenvironment healthy. However, noxious insults to the brain caused by trauma, ischemia or environmental/chemical toxins alter the BBB function to small as well as large molecules e.g., proteins. When proteins enter the CNS fluid microenvironment, development of brain edema occurs due to altered osmotic balance between blood and brain. On the other hand, almost all neurodegenerative diseases and traumatic insults to the CNS and subsequent BBB dysfunction lead to edema formation and cell injury. To treat these brain disorders suitable drug therapy reaching their brain targets is needed. However, due to edema formation or only a focal disruption of the BBB e.g., around brain tumors, many drugs are unable to reach their CNS targets in sufficient quantity. This results in poor therapeutic outcome. Thus, new technology such as nanodelivery is needed for drugs to reach their CNS targets and be effective. In this review, use of nanowires as a possible novel tool to enhance drug delivery into the CNS in various disease models is discussed based on our investigations. These data show that nanowired delivery of drugs may have superior neuroprotective ability to treat several CNS diseases effectively indicating their role in future therapeutic strategies.
Read more: http://www.eurekaselect.com/node/144937/article