Plasma Aß, homocysteine, and cognition  

Oleh:

Viswanathan, A. ; Raj, S. ; Greenberg, S. M.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Neurology (Official Journal of The American Academy of Neurology) vol. 72 no. 03 (Jan. 2009), page 268-272.
Topik: VITAMIN; STROKE; ALZHEIMER DISEASE

Ketersediaan

Perpustakaan FK Nomor Panggil: N11.K.2009.01 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Background: Amyloid-beta protein (Aß) plays a key role in Alzheimer disease (AD) and is also implicated in cerebral small vessel disease. Serum total homocysteine (tHcy) is a risk factor for small vessel disease and cognitive impairment and correlates with plasma Aß levels. To determine whether this association results from a common pathophysiologic mechanism, we investigated whether vitamin supplementation–induced reduction of tHcy influences plasma Aß levels in the Vitamin Intervention in Stroke Prevention (VISP) study. Methods: Two groups of 150 patients treated with either the high-dose or low-dose formulation of pyridoxine, cobalamin, and folic acid in a randomized, double-blind fashion were selected among the participants in the VISP study without recurrent stroke during follow-up and in the highest 10% of the distribution for baseline tHcy levels. Concentrations of plasma Aß with 40 (Aß40) and 42 (Aß42) amino acids were measured at baseline and at the 2-year visit. Results: tHcy levels significantly decreased with vitamin supplementation in both groups. tHcy were strongly correlated with Aß40 but not Aß42 concentrations. There was no difference in the change in Aß40, Aß42 (p = 0.40, p = 0.35), or the Aß42/Aß40 ratio over time (p = 0.86) between treatment groups. Aß measures were not associated with cognitive change. Conclusions: This double-blind randomized controlled trial of vitamin therapy demonstrates a strong correlation between serum tHcy and plasma Aß40 concentrations in subjects with ischemic stroke. Treatment with high dose vitamins does not, however, influence plasma levels of Aß, despite their effect on lowering tHcy. Our results suggest that although tHcy is associated with plasma Aß40, they may be regulated by independent mechanisms.

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