Aberrant expression of nitric oxide synthase III in Alzheimer’s disease: relevance to cerebral vasculopathy and neurodegeneration

  title={Aberrant expression of nitric oxide synthase III in Alzheimer’s disease: relevance to cerebral vasculopathy and neurodegeneration},
  author={Suzanne de la Monte and Bing-xun Lu and Yoon Kyung Sohn and D Etienne and Joanny Kraft and Neema Ganju and Jack R Wands},
  journal={Neurobiology of Aging},

Nitric Oxide Synthase 3-Mediated Neurodegeneration After Intracerebral Gene Delivery

The results suggest that increased cerebral expression of NOS3 causes several molecular abnormalities related to AD-type neurodegeneration, including oxidative stress, mitochondrial dysfunction, and impaired acetylcholine homeostasis.

The AD7c-NTP neuronal thread protein biomarker for detecting Alzheimer's disease.

Results from a number of studies suggest that AD7c-NTP is an excellent biomarker that could be helpful in the routine clinical evaluation of elderly patients at risk for AD.

NO synthase 2 (NOS2) deletion promotes multiple pathologies in a mouse model of Alzheimer's disease

It is shown that NO may be a key factor that connects amyloid and tau pathologies and acts at a junction point between β-amyloid peptide levels, neuronal degeneration, caspase-3 activation, and tAU cleavage.

Nitric Oxide Synthase-3 Overexpression Causes Apoptosis and Impairs Neuronal Mitochondrial Function: Relevance to Alzheimer's-Type Neurodegeneration

NOS3-induced neuronal death is mediated by Mt dysfunction, oxidative injury, and impaired membrane integrity, rather than by NO production, and that neuroprotection from these adverse effects of NOS3 may be achieved by modulating intracellular levels of oxidative stress.

Protective Effects of Adaptation to Hypoxia in Experimental Alzheimer’s Disease

Protective effects of adaptation to intermittent hypobaric hypoxia on the memory, brain neurons, and cerebral blood vessels in rats with experimental AD induced by intracerebral injections of beta-amyloid (Aβ) and mechanisms of these protective effects are focused on.

Ammonia and Alzheimer’s disease

  • N. Seiler
  • Biology
    Neurochemistry International
  • 2002



Aberrant expression of the constitutive endothelial nitric oxide synthase gene in Alzheimer disease.

Investigation of Expression of one of the enzymes responsible for NO synthesis, the constitutive endothelial NO synthase (ceNOS), in brains of AD and Down syndrome patients suggests that aberrant ceNOS translocation and gene regulation may have important roles in the pathogenesis of AD neuritic pathology.

Inducible nitric oxide synthase in tangle-bearing neurons of patients with Alzheimer's disease

Human neurons can express NOS2 in vivo, and the high-output pathway of NO production may contribute to pathogenesis in AD.

Neuritic sprouting with aberrant expression of the nitric oxide synthase III gene in neurodegenerative diseases

Amyloid β‐Protein Induces the Cerebrovascular Cellular Pathology of Alzheimer's Disease and Related Disorders a

Together, these studies provide evidence that Aβ contributes to the onset and progression of the cerebrovascular pathology associated with AD and related disorders and suggests the mechanism involves a molecular cascade with a novel product‐precursor relationship that results in the adverse production and accumulation of Aβ.

Cerebrovascular Pathology Contributes to the Heterogeneity of Alzheimer's Disease.

Since the AD and AD+CVA groups had similar degrees of dementia, the results suggest that cerebral vascular lesions in regions typically destroyed by AD may contribute to the clinical manifestations of AD.

Correlates of p53- and Fas (CD95)-mediated apoptosis in Alzheimer's disease

In vivo vascular damage, leukocyte activation and inflammatory response induced by beta-amyloid.

Using intravital microscopy it is demonstrated that in vivo administration of beta-amyloid produces extensive vascular disruption including endothelial and smooth muscle damage, adhesion and migration of leukocytes across arteries and venules.

Alterations of the blood-brain barrier and glial cells in white-matter lesions in cerebrovascular and Alzheimer's disease patients.

Dysfunction of the blood-brain barrier is more prominent in white-matter lesions seen in ischemic CVD than in AD and may have a role in the pathogenesis of cerebrovascular white- Matter lesions.

β-Amyloid-mediated vasoactivity and vascular endothelial damage

It is demonstrated here that β-amyloid interacts with endothelial cells on blood vessels to produce an excess of superoxide radicals, with attendant alterations in endothelial structure and function, which suggest a normal vasoactive role for β- amyloid as well as a mechanism by which β-Amyloid may play a role in vascular abnormalities and neurodegeneration mediated by free radicals.

Regressive changes of astroglia in white matter lesions in cerebrovascular disease and Alzheimer’s disease patients

Abstract The pathogenesis of white matter lesions, which are frequently found in ischemic cerebrovascular disease and Alzheimer’s disease, remains unclear. Using light and electron microscopic