Production of autoantibodies to glutamate during Alzheimer's dementia.

Increased production of autoantibodies to glutamate was found in blood plasma from patients with Alzheimer's dementia. The content of autoantibodies to glutamate in patients with early-onset Alzheimer's disease was much lower than in those with late-onset Alzheimer's disease (1.40+/-0.07 and 1.80+/-0.07 arb. units, p<0.001). The level of autoantibodies to glutamate in patients with mixed - Alzheimer's disease was 1.60+/-0.01 arb. units.

Induction of autoantibodies to glutamate in patients with Alzheimer's disease.

Autoantibodies to glutamate were found in blood plasma from patients with Alzheimer's disease. The content of autoantibodies to glutamate in blood plasma from patients with moderate and severe dementia was 2-fold higher compared to patients with mild dementia.

Autoimmune responses to amyloid structures of Abeta(25-35) peptide and human lysozyme in the serum of patients with progressive Alzheimer's disease.

We have found an increased level of serum antibodies to the prefibrillar structures of both Abeta(25-35) peptide and human lysozyme in Alzheimer's disease (AD) patients compared to age-matched controls, indicating that autoimmunity is implicated in AD. In the serum of AD patients with a long-term duration (>15 years) the titer of serum antibodies to aggregates of Abeta(25-35) peptide increased by approximately 5-fold, whilst the antibody titer to lysozyme protofilaments decreased by approximately 8-fold compared to patients with AD duration of <5 years. The content of immunoglobulins of the A, G and M types declined, particularly in AD duration of >15 years. An increase in the concentration of immune complexes and higher lysozyme activity was detected in the serum of all patients and this was suggestive of an inflammatory reaction. We propose that the autoimmune response to different amyloid structures in AD can be viewed as a clearance pathway targeting amyloid development. Autoimmune response can be exploited as a marker of ongoing protein aggregation and hence be used as a diagnostic feature of AD.

Phagocytic activity and state of bactericidal systems in polymorphonuclear leukocytes from patients with Alzheimer's disease.

Phagocytic activity of peripheral blood neutrophils underwent phase changes in patients with Alzheimer's disease. Neutrophils retained the ability to engulf microbes, but their digestive activity decreased at the early stage of Alzheimer's disease. At the late stage we observed a decrease in the count of phagocytizing neutrophils, reduction of myeloperoxidase activity, and increase in the content of cationic proteins.

Induction of immune complexes and autoantibodies to serotonin and dopamine in patients with Alzheimer's disease.

Plasma concentration of immune complexes and antibodies to serotonin and dopamine were higher in patients with Alzheimer's disease compared to mentally healthy volunteers of the same age. Plasma concentrations of antibodies to serotonin and dopamine decreased with the increase in the duration of this disease.

Genetic linkage studies suggest that Alzheimer's disease is not a single homogeneous disorder.

Alzheimer's disease, a fatal neurodegenerative disorder of unknown aetiology, is usually considered to be a single disorder because of the general uniformity of the disease phenotype. Two recent genetic linkage studies revealed co-segregation of familial Alzheimer disease with the D21S1/S11 and D21S16 loci on chromosome 21. But two other studies, one of predominantly multiplex kindreds with a late age-of-onset, the other of a cadre of kindreds with a unique Volga German ethnic origin, found absence of linkage at least to D21S1/S11. So far it has not been possible to discern whether these conflicting reports reflect aetiological heterogeneity, differences in methods of pedigree selection, effects of confounding variables in the analysis (for example, diagnostic errors, assortative matings), or true non-replication. To resolve this issue, we have now examined the inheritance of five polymorphic DNA markers from the proximal long arm of chromosome 21 in a large unselected series of pedigrees with familial Alzheimer's disease. Our data suggest that Alzheimer's disease is not a single entity, but rather results from genetic defects on chromosome 21 and from other genetic or nongenetic factors.

Effect of light quality on the organization of photosynthetic electron transport chain of pea seedlings.

The activity of NADP and O(2) photoreduction by water is essentially higher in chloroplasts isolated from pea seedlings (Pisum sativum L.) grown under blue light as compared with that from plants grown under red light. In contrast, the photoreduction of NADP and O(2) with photosystem I only is practically the same or even lower in chloroplasts isolated from plants grown under blue light. The addition of plastocyanin does not affect the rate or the extent of NADP photoreduction by water in the chloroplasts isolated from plants grown under blue light, whereas it sharply activates NADP reduction in the chloroplasts isolated from plants grown under red light. The extent of the light-induced oxidation of cytochrome f is appreciably higher in chloroplasts isolated from plants grown under blue light. Cytochrome b(559) plays the predominant role in the oxidoreductive reactions of these chloroplasts. Furthermore, the fluorescence measurements indicate more effective transfer of excitation energy from chlorophyll to the photosystem II reaction center in chloroplasts isolated from plants grown under blue light.The data reported are interpreted in terms of differential rates of electron transport from water in the two chloroplast preparations.