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PubMed1986

Are Alzheimer neurofibrillary tangles insoluble polymers?

The two methods currently available for the bulk isolation of Alzheimer tangles of paired helical filaments (PHF) are based on a brief treatment of a neuronal-enriched preparation with sodium dodecyl sulfate (SDS) (Method I) and on heating of whole brain homogenate with SDS and beta-mercaptoethanol (Method II). PHF were isolated from the same Alzheimer brain by these two methods, subjected to SDS-polyacrylamide gel electrophoresis and immuno-labelled with monoclonal antibodies to PHF after transferring from the gel to nitrocellulose paper. The PHF isolated by method I revealed the presence of 45 kilodalton to 62 kilodalton PHF polypeptides, whereas the PHF isolated by method II were excluded from the gel. However, PHF isolated by both methods were digested with proteinase-K, though the degradation of PHF of method I was considerably more rapid than that of PHF isolated by method II. These findings should establish that the solubility of PHF might depend on the methods employed for their isolation and that they might not be insoluble polymers of covalently crosslinked polypeptides which accumulate irreversibly in the brain of patients with Alzheimer disease.

Alzheimer Disease↗
PubMed1984

Ultrastructure of paired helical filaments of Alzheimer's neurofibrillary tangle.

Isolated paired helical filaments (PHF) of Alzheimer's disease and senile dementia of the Alzheimer type (AD/SDAT) were studied by negative stain techniques and electron microscopy (EM). The helical structure of the PHF was confirmed by tilt analysis of negatively stained isolated PHF. A substructure of four protofilaments, each 3-5 nm in diameter, was also observed. A comparison of PHF substructure, neurofilaments and microtubules, revealed no similarity among the three structures.

Aged↗
PubMed1997

The loss of GluR2(3) immunoreactivity precedes neurofibrillary tangle formation in the entorhinal cortex and hippocampus of Alzheimer brains.

Double-immunolabeling techniques were employed to examine the distribution of GluR2(3) subunits and markers of early cytoskeletal changes (mab MC1) within the entorhinal cortex (EC) and hippocampus of cases with varying degrees of Alzheimer disease (AD) pathology (stages I-VI by Braak and Braak). In addition near-adjacent tissue sections were double-immunolabeled using antibodies against GluR2(3) and a marker of normal neuronal cytoskeleton (MAP2). In those cases classified as stages I-II, most layer II neurons of the EC and pyramidal neurons in the CA1/subiculum were double-labeled with GluR2(3) and MAP2. An occasional MC1-labeled cell was observed, yet in no instance were these neurons double-labeled with GluR2(3). In cases with moderate AD pathology (stages III-IV), layer II of the EC and CA1/subiculum were characterized by a substantial loss of GluR2(3)-labeled neurons, while many were still immunoreactive to MAP2. Notably, the loss of GluR2(3) immunolabeling was accompanied by an increasing number of MC1-positive neurons. In no instance were GluR2(3) and MC1 co-localized within the same neuron. In cases with severe AD pathology (stages V-VI), the EC and CA1/subiculum were almost completely devoid of GluR2(3)-positive neurons. MAP2-labeled neurons also were reduced in number. In contrast, both regions contained an abundance of MC1-positive cells. That GluR2(3) and MC1 are not observed in the same neuron, together with the observation that the number of GluR2(3)-labeled neurons decreases as the number of MC1-positive cells increases, suggest that a loss of GluR2(3) immunolabeling precedes the appearance of MC1 immunolabeling.

Aged↗
PubMed1982

Senile plaques and neurofibrillary tangles of the Alzheimer type in nondemented individuals at presenile age.

100 unselected brains of patients dying at the ages of 55--64 years were examined for the presence of Alzheimer type changes. These changes were found in 25 brains. This number is lower than that in a comparable investigation from Japan, but it is clearly above the number found in selected nondemented patients from England. Although none of the patients had suffered from an easily recognizable presenile dementia, an important proportion of them had been noted for unusual psychology. The occurrence of Alzheimer type changes was not dependent on the diseases the patients had suffered from.

Alcoholism↗