Significats de senile plaques en anglès

Immunohistochemical analysis showed that C1q protein was localized in senile plaques in the AD brain.

At light microscopy, acid phosphatase and APP colocalized to the same cell processes in senile plaques.

These observations are important because increased tau accumulation in senile plaques can be a hallmark of AD.

PS1 immunoreactivity was present in the neuritic component of senile plaques as well as in neurofibrillary tangles.

On the other hand it is known that apoE co-purifies with A beta biochemically extracted from senile plaques.

This study presents evidence for plasma membrane abnormalities of the dystrophic neurites in senile plaques of Alzheimer's disease.

Alzheimer's disease (AD) is characterized by the presence of amyloid-positive senile plaques and tau-positive neurofibrillary tangles.

The present results suggest that C1q protein in senile plaques originates is endogenously produced in the AD brain.

Abundant senile plaques and neurofibrillary tangles in certain brain regions constitute the major neuropathological characteristics of Alzheimer's disease.

AD is characterized by progressive neuronal death associated with neuropathological lesions consisting of neurofibrillary tangles and senile plaques.

Numerous proteins have been identified immunohistochemically to be associated with senile plaques, where A beta is the major constituent.

Microglia was involved in different types of senile plaques and often were associated closely with APP immunoreactive neurites and neurons.

These intensely staining cells were frequently observed surrounding senile plaques, but represented a small proportion of the total astrocytic population.

The microglia and astrocytes have quiescent morphology compared with those associated with senile plaques and other lesions such as ischemia.

Alzheimer's disease (AD) is characterized pathologically by the abundance of senile plaques and neurofibrillary tangles in the brain.

However, behavioral decline begins before the appearance of significant numbers of senile plaques, suggesting that other factors may interfere with cognition.