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Home: Papers of the Week
Annotation


Calon F, Lim GP, Yang F, Morihara T, Teter B, Ubeda O, Rostaing P, Triller A, Salem N, Ashe KH, Frautschy SA, Cole GM. Docosahexaenoic acid protects from dendritic pathology in an Alzheimer's disease mouse model. Neuron. 2004 Sep 2;43(5):633-45. PubMed Abstract

  
Comments on Paper and Primary News
  Primary News: Fish Oil Swims Ahead in Dietary Brain Protection Race

Comment by:  Colin Meyer
Submitted 8 September 2004  |  Permalink Posted 8 September 2004

With regard to the recent focus upon a diet rich in fish and its protective effect against Alzheimer's disease, please allow me to point out that the assumption that this is attributable to omega-3 fatty acids may be misguided.

There are two groups of foods that provide unusually high levels of silicic acid. Thin-skinned fruits such as grapes and blueberries evaporate moisture through the epidermous, thereby concentrating the solubilized silicon within the fruit.

And over the eons silicic acid endlessly concentrates in the oceans in the same manner as salt.

Thus, the two food groups from which consumers can expect to elevate their blood levels of silicic acid are thin-skinned fruit and marine seafood. And the two foods for which epidemiological studies have indicated a protective effect against Alzheimer's disease are red wine and fish.

View all comments by Colin Meyer


  Primary News: Fish Oil Swims Ahead in Dietary Brain Protection Race

Comment by:  Mary Reid
Submitted 9 September 2004  |  Permalink Posted 10 September 2004

Does this study support a dissociation between LTP and spatial memory?

Itokazu and colleagues (1) report that DHA inhibits the induction of long-term potentiation in the CA1 area in rats, as is shown to be the case for Aβ in many studies.

I'd also be interested in the answer to the question proposed by Lennart Mucke and Robert Pitas as to whether production of Aβ is affected by DHA.

Reference:
Itokazu N, Ikegaya Y, Nishikawa M, Matsuki N. Bidirectional actions of docosahexaenoic acid on hippocampal neurotransmissions in vivo. Brain Res. 2000 Apr 17;862(1-2):211-6. Abstract

References:


View all comments by Mary Reid

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REAGENTS/MATERIAL:

Seventeen-month-old male and female Tg2576 Tg(+) and Tg(−) (Taconic) were used in this study.

Antibodies used for this study were anti-Drebrin (clone M2F6, MBL), anti-PSD-95 (Upstate Biotech), anti-GFAP (Sigma), anti-SNAP-25 (Sternberger Monoclonals), anti-p85 (Stressgen and BD-Pharmingen); anti-neuronal nuclei (NeuN), synaptophysin (MAB368), and anti-actin (Chemicon International); anti-phosphoAkt, anti-phospho-BAD (ser136) and anti-total BAD (Cell Signaling) and anti-14-3-3 (Santa Cruz Biotechnology). Affinity purified anti-fractin rabbit polyclonal antibody was developed and characterized in our laboratory.

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