The distribution of casein kinase 1 delta (Cki delta) was studied by immunohistochemistry and correlated with other pathological hallmarks in Alzheimer's disease (AD), Down syndrome (DS), progressive supranuclear palsy (PSP), parkinsonism dementia complex of Guam (PDC), Pick's disease (PiD), pallido-ponto-nigral degeneration (PPND), Parkinson's disease (PD), dementia with Lewy bodies (DLB), amyotrophic lateral sclerosis (ALS), and elderly controls. Cki delta was found to be associated generally with granulovacuolar bodies and tau-containing neurofibrillary tangles in AD, DS, PSP, PDC, PPND, and controls, and Pick bodies and ballooned neurons in PiD. It was not associated with tau-containing inclusions in astroglia and oligodendroglia in PPND, PSP, and PDC. It was also not associated with tau-negative Lewy bodies in PD and DLB, Hirano bodies in PDC, Marinesco bodies in PD, AD, and controls and "skein"-like inclusions in anterior motor neurons in ALS. The colocalization of the kinase Cki delta and its apparent substrate tau suggests a function for Cki delta in the abnormal processing of tau.

Aged↗

PubMedDate not supplied

The pentraxins: possible role in Alzheimer's disease and other innate inflammatory diseases.

Two short pentraxins, C-reactive protein and amyloid P, are found in association with the senile plaques and neurofibrillary tangles of Alzheimer disease (AD). Formerly thought to be made primarily if not solely in liver, recent work has shown that they are made not only in the brain but in other tissues such as heart and arteries. Their synthesis is markedly upregulated in affected brain regions in AD. Since they are known to activate the complement cascade in an antibody-independent fashion and chronic activation can cause destruction of host tissue, these pentraxins may be important initiators of an autodestructive process. As such, they may be prime targets for therapeutic intervention.

Acute-Phase Proteins↗

PubMedDate not supplied

Tubulin immunopositive structures resembling intracellular neurofibrillary tangles.

Tau protein promotes microtubule assembly. When aberrantly phosphorylated, it forms the core of neurofibrillary tangles (NFTs). We investigated by immunohistochemistry whether microtubules might also be involved in NFT formation. We found beta-tubulin immunoreactive NFT-like structures in Alzheimer disease, and, more frequently, in the parkinsonism dementia complex of Guam (bodig disease) and Down Syndrome. The beta-tubulin immunoreactive structures were intracellular and appeared at an early stage of tangle development. This may indicate an involvement of tubulin in NFT formation.

Aged↗

PubMedDate not supplied

On the survival time of a tangled neuron in the hippocampal CA4 region in parkinsonism dementia complex of Guam.

In diseases such as the Parkinson dementia complex of Guam (PDC) or Alzheimer's disease, susceptible neurons develop intracellular tangles (iNFTs) and then die, leaving behind extracellular tangles (eNFTs). We performed counts of healthy neurons, iNFTs, and eNFTs in the hippocampus of Guamanian Chamorros who were neurologically normal or who suffered from PDC. The total of surviving and dead neurons in the CA4 region was remarkably constant from case to case, indicating that eNFTs are not phagocytosed. Since cases of recent PDC showed only marginal tangle formation in CA4, we concluded that tangle development in CA4 commenced close to the onset of the disease. Based on this assumption, as well as the further assumption that the average rate of tangle development and the average lifetime of a tangled neuron do not alter as the disease progresses, we derived equations to determine the average lifetime of tangled neurons. The results varied from 0.13 years for the most rapidly progressing case to 7.98 years for the most slowly developing case. The average for 8 cases was 2.51 years.

Adult↗

PubMedDate not supplied

The dental hygienist as sole proprietor: a new concept in preventive dentistry.

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