Alzheimer’s brain

In studies in Alzheimer s brain, in vitro induction of lipid peroxidation by iron is more intense than in control cortical samples (Andorn et al., 1990 Subbarao et nL, 1990 McIntosh et al., 1991). The 21-aminosteroid U-74500A has been shown to effectively inhibit iron-induced lipid peroxidation in Alzheimer s brain samples (Subbarao et al., 1990). 

Andorn, A.C., Britton, R.S. and Bacon, B.R. (1990). Evidence that lipid peroxidation and total iron are increased in Alzheimer s brain. Neurobiol. Aging 11, 316-320. 

Figure 8.3 Transient signals of 63 Cu and 65Cu in protein spots of Alzheimer s brain samples measured by LA-ICP-MS (isotopic-enriched 65Cu spike solution was doped to the gel after 2D gel electrophoresis). (J. Su. Becker et al, Int. ). Mass Spectrom., 242, 135 (2005). Reproduced by permission of The Royal Society of Chemistry.)...

Although it has been postulated that the presence of amyloid protein in the Alzheimer s brain could be specifically involved in the causation of the... 

Westlake TM, Howlett AC, Bonner II, Matsuda LA, Herkenham M. 1994. Cannabinoid receptor binding and messenger RNA expression in human brain An in vitro receptor autoradiography and in situ hybridization histochemistry study of normal aged and Alzheimer s brains. Neuroscience 63 637-652. 

Figure 8.3 Transient signals of and Cu in protein spots of Alzheimer s brain samples measured...

Reduced in Alzheimer s brains and CSF. Elevated levels following tacrine and rivastigmine treatments are correlated to improved cognition Attenuates disease progression following MPTP exposure (neuroprotective) Overexpressed and involved... 

Markesbery, WR University of Kentucky Lexington, KY Oxidative, antioxidant and trace element studies in the alzheimer s brain. National Institute on Aging... 

Mitochondrial DNA deletions in Alzheimer s brains A review. Alzheimers Dement... 

Evidence for CB2 receptor expression has not been found in normal human CNS however, CB2 has been found in Alzheimer s brains (Benito et al. 2003). CB2 immunoreactivity was selectively expressed in microglia associated with neuritic plaques, suggesting that modulation of their activity may have therapeutic implications (Benito et al. 2003). 

Increased phosphoryl-3-choline in post-mortem Alzheimer s brain. Lancet i 517. 

M. Ono, Development of positron-emission tomography/single-photon emission computed tomography imaging probes for in vivo detection of beta-amyloid plaques in Alzheimer s brains, Chem. Pharm. Bull. (Tokyo) 57 (10) (2009) 1029-1039. 

Banks, W.A. 2004. The source of cerebral insulin. Eur. J. Pharmacol. 490 5-12 Baiger, S.W. and Mattson, M.P. 1997. Isoform-specific modulation by apohpoprotein E of the activities of secreted P-amyloid precursor protein. J. Neurochem. 69 60-67 Baudier, J. and Cole, R.D. 1987. Phosphorylation of tau proteins to a state like that in Alzheimer s brain is catalyzed by a calcium/calmoduUn-dependent kinase and modulated by phospholipids. J. Biol. Chem. 262 17577-17583... 

Neurodegenerative diseases are characterized by the persistent loss of neuronal activity which results in disorders related to the central nervous system (CNS). The various degenerative disorders include Parkinson s, Alzheimer s, brain cancer, etc. These diseases are a big threat to the global population, which has been estimated to be 1.5 billion people suffering from CNS disorders. The existing therapeutic possibilities are still limited. The worldwide market for CNS therapeutics was about 57 billion USD in 2005 and has been forecasted to reach 133 billion USD by the year 2018, primarily driven by increase in disease prevalence rates due to the aging population. 

Shankar GM, Li S, Mehta TH, et al. Amyloid-beta protein dimers isolated directly from Alzheimer s brains impair synaptic plasticity and memory. Nat Med. 2008 14(8) 837-842. 

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