We investigated the influence of the polyunsaturated docosahexaenoic acid (22:6n-3; DHA) on the constitutive expression of choline acetyltransferase (ChAT) in native and induced expression in differentiated cholinergic cells NG108-15 grown in serum-free medium. Elimination of serum-derived trophic support resulted in growth arrest and a strong decrease of ChAT activity. In either conditions, DHA largely rescued general indicators of cell growth and function, and partially prevented the decrease of ChAT activity. However, the maximal effect on general cell state in native and differentiated cells, and ChAT activity in native cells, was reached at or below 10 mumol/l of DHA. In contrast, maximal induction of ChAT activity in differentiated cells required about six times higher concentrations of DHA. These data thus demonstrate stimulatory effect of DHA on ChAT activity that is independent of its general cell protective properties.

• MeSH
• Cell Division drug effects   MeSH
• Cell Line MeSH
• Choline O-Acetyltransferase metabolism   MeSH
• Culture Media, Serum-Free MeSH
• Docosahexaenoic Acids pharmacology   MeSH
• Humans MeSH
• Oxidative Stress MeSH
• Check Tag
• Humans MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Names of Substances
• Choline O-Acetyltransferase MeSH
• Culture Media, Serum-Free MeSH
• Docosahexaenoic Acids MeSH

It is generally accepted that the crucial events in the pathogeny of Alzheimer's disease (AD) are the increased accumulation of amyloidogenic peptides derived from amyloid precursor protein and the harmful actions of these peptides on neurons, which bring about neurodegeneration. The enhanced beta-amyloid accumulation is known to be caused by mutations of specific genes in patients who suffer from the familial (hereditary) form of AD but who represent just a minor group within the total population of AD patients. The reasons for beta-amyloid accumulation are not known in the much larger group of patients with the sporadic form of the disease. A biochemical feature common to either form of the disease is the preferential atrophy and degeneration of cholinergic neurons, which is probably responsible for much of the cognitive decline characteristic of the disease. We present an overview of recent investigations on the interactions between beta-amyloid and cholinergic neurons.

• MeSH
• Amyloid beta-Peptides metabolism   MeSH
• Amyloid beta-Protein Precursor metabolism   MeSH
• Cholinergic Fibers physiology   MeSH
• Phenotype MeSH
• Glucose metabolism   MeSH
• Humans MeSH
• Neurons physiology   MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Research Support, Non-U.S. Gov't MeSH
• Review MeSH
• Names of Substances
• Amyloid beta-Peptides MeSH
• Amyloid beta-Protein Precursor MeSH
• Glucose MeSH