Targeting therapy for homocysteic acid in the blood represents a potential recovery treatment for cognition in Alzheimer's disease patients.

At present, we have no reliable means of recovering cognitive impairment in Alzheimer's disease (AD) patients. We hypothesized that homocysteic acid (HA) in the blood might represent one such pathogen that could be excreted into the urine. Since DHA is known to reduce circulating levels of homocysteine, and since exercise attenuates this effect, it follows that supplementation of the diet with DHA, along with increased levels of physical activity, may help to reduce cognitive impairment in AD patients.

Urinary homocysteic acid levels correlate with mini-mental state examination scores in Alzheimer's disease patients.

Homocysteic acid (HA) has been suggested as a pathogen in a mouse model of Alzheimer's disease (AD), 3xTg-AD. However, it is not established whether HA is involved in humans. We investigated the relationship between urinary HA levels and Mini-Mental State Examination (MMSE) scores in AD patients (n = 70) and non-AD controls (n = 34).

Prolonged stress will induce Alzheimer's disease in elderly people by increased release of homocysteic acid.

Recently, many papers have reported the physiological functions of amyloid beta and amyloid precursor protein (APP). In particular, one of its functions is of importance for synaptic plasticity. Extracellular amyloid beta may suppress synaptic plasticity or inhibit long-term potentiation (LTP) from outside the cell.