Docosahexaenoic acid protects from dendritic pathology in an Alzheimer's disease mouse model.

By F. Calon, Giselle P. Lim, Fusheng Yang, T. Morihara, B. Teter, O. Ubeda, Phillippe Rostaing, A. Triller, N. Salem, K. Ashe and 2 more. Neuron, 2004

747 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Nutrition and Dietetics, Physiology

View Paper: https://www.semanticscholar.org/paper/06b18efbd828a9cb66f6158056599fb14d6b0230

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. P. Lacor
2. P. Velasco
3. Undurti N. Das
4. W. Klein
5. K. Viola

In Nutrition and Dietetics

1. K. Tucker
2. Undurti N. Das

In Physiology

1. K. Viola
2. P. Velasco
3. P. Lacor
4. W. Klein
5. Maria C. F. Buniel
6. D. Selkoe

Citations in the corpus

• Omega-3 fatty acid treatment in 174 patients with mild to moderate Alzheimer disease: OmegAD study: a randomized double-blind trial. (2006, neutral): “Female sex, No. (%) 51 (57) 39 (46) 10 (71) 10 (63) Age, y 72.6 ± 9.0 72.9 ± 8.6 77.0 ± 8.2 78.2 ± 7.5 Diabetes, No. (%) 10 (13) 4 (6) 1 (8) 0 Smoking, No. (%) 7 (10) 6 ( 9 ) NA NA APOE4, No. (%) 0 21 (24) 28 (33) 9 (57) 5 (31) 1 46 (52) 39 (46) 4 (22) 6 (31) 2 22 (25) 18 (21) 1 (7) 5 (31)”
• Plasma phosphatidylcholine docosahexaenoic acid content and risk of dementia and Alzheimer disease: the Framingham Heart Study. (2006, background): “Recent studies in a mouse model of Alzheimer disease support these concepts.(25) In the future, it will also be important to determine whether combined dietary supplementation with DHA can decrease further mental deterioration in patients with established dementia.”
• Defects in IGF-1 receptor, insulin receptor and IRS-1/2 in Alzheimer's disease indicate possible resistance to IGF-1 and insulin signalling. (2010, background): “Regulatory p85 I3-kinase subunits have already been shown to be reduced n AD (Calon et al., 2004).”
• Aβ Oligomer-Induced Aberrations in Synapse Composition, Shape, and Density Provide a Molecular Basis for Loss of Connectivity in Alzheimer's Disease (2007, background): “Tg mice also exhibit decreased drebrin (Calon et al., 2004), consistent with loss of spines.”
• Essential fatty acids: biochemistry, physiology and pathology (2006, background): “Both LXs and NPD1 enhanced wound healing [95], and promoted brain cell survival via the induction of anti-apoptotic and neuroprotective gene-expression programs that suppress Aβ42-induced neurotoxicity [77, 78].”