Treatment Of Alzheimer's Disease In Mice With Anti-Homocysteic Acid Antibody

Main Category: Alzheimer's / Dementia
Article Date: 20 Jan 2010 - 0:00 PDT

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Recent research reporting the clinical inefficacy of amyloid treatment for Alzheimer's disease has introduced some confusion into this research field, and studies should be careful take into account the different pathogenic effects of amyloid between Alzheimer's in a mouse model and in humans. Amyloid treatment has been shown to have some success in restoring the cognitive ability of mice; however, in human studies, this success has not been replicated.

In a new study published in PLOS ONE, Professor Tohru Hasegawa of the Saga Woman Junior College, Japan, and colleagues report that homocysteic acid (HA), which is metabolized from homocysteine or methionine, is the pathogen for Alzheimer's disease and that this pathogen works in conditions of amyloid toxicity. The researchers confirmed this pathogenic action of HA using a new HA vaccine for 3xTg-AD model mice (APP, Presenilin and Tau).

The model mice showed higher HA levels before amyloid-induced Alzheimer's pathological change. Then, the HA vaccine led to the recovery of the cognitive disability of model mice independently from amyloid toxicity.

According to the researchers, humans excrete HA into urine at levels 1000 times higher than mice. This means humans have a much higher HA toxicity than mice. The amyloid treatment decreases the amyloid levels in the mouse's brain and then HA toxicity appears in mice. HA levels in mice are low resulting in weak HA toxicity. However, HA level are higher in humans than in mice. HA consequently displays strong toxicity in Humans.

The authors conclude that the pathogenic effect of HA in humans with Alzheimer's disease needs to be considered, in addition to amyloid treatment.

Funding:

This experiment was supported by Arfresa Pharmcology (http://www.alfresa-pharma.co.jp). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Competing interests:

The authors have declared the following competing interests: "N.M is employed by Kyudo Ltd; this company had no role in this study design, data collection and analysis, decision to publish, or preparation of this manuscript. All other authors declare no competing interests. Parts of the experiment, such as feeding model mice were supported by Arfresa Pharmcology (http://www.alfresa-pharma.co.jp)."

Citation:

"Treatment of Alzheimer's Disease with Anti-Homocysteic Acid Antibody in 3xTg-AD Male Mice."
Hasegawa T, Mikoda N, Kitazawa M, LaFerla FM (2010)
PLoS ONE 5(1): e8593. doi:10.1371/journal.pone.0008593

Source
PLoS ONE

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