(2000). AK: Oxidative stress in Alzheimer’s disease. Biochim Biophys Acta
(2000). Akt/Protein kinase B up-regulates Bcl-2 expression through cAMP-response element-binding protein.
(2002). Amyloid beta -peptide inhibition of the PKA/CREB pathway and longterm potentiation: reversibility by drugs that enhance cAMP signaling. Proc Natl Acad Sci USA
(1997). Amyloid beta protein toxicity and oxidative stress in Alzheimer’s disease. Cell Tissue Res
(2000). Apoptosis in neurodegenerative disorders.
(2004). Arancio O: Persistent improvement in synaptic and cognitive functions in an Alzheimer mouse model after rolipram treatment.
(2002). Arendash GW: Behavioral characterization of the Tg2576 transgenic model of Alzheimer’s disease through 19 months. Physiol Behav
(2004). Astrocyte apoptosis: implications for neuroprotection. Prog Neurobiol
Barco A: CREB’s control of intrinsic and synaptic plasticity: implications for CREB-dependent memory models.
(2001). Caspases, apoptosis, and Alzheimer disease: causation, correlation, and confusion.
(2001). CM: Recovery and expression of messenger RNA from postmortem human brain tissue. Mod Pathol
(2004). Cotman CW: Beta-amyloid peptide at sublethal concentrations downregulates brain-derived neurotrophic factor functions in cultured cortical neurons.
(2004). Cotman CW: Caspase-cleavage of tau is an early event in Alzheimer disease tangle pathology.
(1996). Coupling of the RAS-MAPK pathway to gene activation by RSK2, a growth factor-regulated CREB kinase. Science
(2000). CREB couples neurotrophin signals to survival messages. Neuron
(2001). CW: Beta-amyloid-(1-42) impairs activity-dependent cAMP response element-binding protein signaling in neurons at concentrations in which cell is not compromised.
(1994). DA: A model for beta-amyloid aggregation and neurotoxicity based on free radical generation by the peptide: relevance to Alzheimer’s disease.
(2002). DD: Function and regulation of CREB family transcription factors in the nervous system. Neuron
(1996). DR: Induction of CRE-mediated gene expression by stimuli that generate long-lasting LTP in area CA1 of the hippocampus. Neuron
(1998). DR: Stimulation of cAMP response element (CRE)-mediated transcription during contextual learning. Nat Neurosci
(1991). Effects of inorganic lead on the differentiation and growth of cultured hippocampal and neuroblastoma cells. Neurotoxicology
(2004). et al: Altered mitogenactivated protein kinase signaling, tau hyperphosphorylation and mild spatial learning dysfunction in transgenic rats expressing the betaamyloid peptide intracellularly in hippocampal and cortical neurons. Neuroscience
FH: Mechanisms underlying inflammation in neurodegeneration.
(1998). G: b-Amyloid fibrils activate parallel mitogen-activated kinase pathways in microglia and THP1 monocytes.
(1994). Greenberg ME: CREB: a mediator of long-term memory from mollusks to mammals. Cell
(1999). Greenberg ME: CREB: a stimulus-induced transcription factor activated by a diverse array of extracellular signals. Annu Rev Biochem
(2005). Helpern JA: Histological colocalization of iron in Abeta plaques of PS/APP transgenic mice. Neurochem Res
(2009). Identification of compounds that potentiate CREB signaling as possible enhancers of long-term memory.
(2006). Inflammation in Alzheimer disease: driving force, bystander or beneficial response? Nat Med
(1997). Iron accumulation in Alzheimer disease is a source of redox-generated free radicals. Proc Natl Acad Sci USA
(1997). JL: Antisense oligodeoxynucleotide-mediated disruption of hippocampal cAMP response element binding protein levels impairs consolidation of memory for water maze training. Proc Natl Acad Sci USA
(1991). JW: BDNF mRNA is decreased in the hippocampus of individuals with Alzheimer’s disease. Neuron
(2006). L: Differential regulation of c-jun and CREB by acrolein and 4-hydroxynonenal. Free Radic Biol Med
(1991). L: The Consortium to Establish a Registry for Alzheimer’s Disease (CERAD). Part II. Standardization of the neuropathologic assessment of Alzheimer’s disease. Neurology
(2004). Landfield PW: Incipient Alzheimer’s disease: microarray correlation analyses reveal major transcriptional and tumor suppressor responses. Proc Natl Acad Sci USA
(2005). Markesbery WR: Evidence of increased oxidative damage in subjects with mild cognitive impairment. Neurology
(2005). MJ: Comparative analysis of cortical gene expression in mouse models of Alzheimer’s disease. Neurobiol Aging
(1989). Montminty MR: Cyclic AMP stimulates somatostatin gene transcription by phosphorylation of CREB at Serine 133. Cell
Obrietan K: CREB: a multifaceted regulator of neuronal plasticity and protection.
(1997). Ogihara T: Elevated amyloid beta protein(1-40) level induces CREB phosphorylation at serine-133 via p44/42 MAP kinase (Erk1/2)-dependent pathway in rat pheochromocytoma PC12 cells. Biochem Biophys Res Commun
(2003). Pugazhenthi S: Cytokine-mediated downregulation of the transcription factor CREB in pancreatic beta -cells.
(2001). R: A gene expression profile of Alzheimer’s disease.
(1991). Rat hippocampal neurons in low-density culture. In Culturing Nerve cells. Edited by:
(1999). Reusch JE-B: Insulin-like growth factor-I induces bcl-2 promoter through the transcription factor cAMP-response element binding protein.
(1999). Reusch JE: Insulin-like growth factor I-mediated activation of the transcription factor cAMP response element-binding protein in PC12 cells. Involvement of p38 mitogen-activated protein kinase-mediated pathway.
(2003). Reusch JE: Oxidative stress-mediated downregulation of bcl-2 promoter in hippocampal neurons.
(1994). RH: Nuclear protein CBP is a coactivator for the transcription factor CREB. Nature
(2001). SG: Agedependent changes in brain, CSF, and plasma amyloid (beta) protein in the Tg2576 transgenic mouse model of Alzheimer’s disease.
(2001). Signatures of hippocampal oxidative stress in aged spatial learning-impaired rodents. Neuroscience
(1993). Significant reductions in synapsin but not synaptophysin specific activity in the brains of some schizophrenics. Biol Psychiatry
(1999). The A beta peptide of Alzheimer’s disease directly produces hydrogen peroxide through metal ion reduction. Biochemistry