We quantified the number of neurons, senile plaques, and neurofibrillary tangles in a high-order association cortex to evaluate the link between dementia, neuronal loss, and neuropathological findings in Alzheimer's disease (AD). Using statistically unbiased, stereological counting techniques, we examined the superior temporal sulcus in 34 AD patients and 17 non-demented control volunteers. In non-demented control patients, the quantity of superior temporal sulcus neurons remained constant from the sixth to the ninth decade. More than half of the neurons in AD were gone. Both neuronal loss and neurofibrillary tangles grew in tandem with the length and severity of the illness, although neuronal loss outweighed neurofibrillary tangle accumulation by a factor of many.
<h3>What is Neurofibrillary ?</h3>
Inside the brain's cells are twisted fibers that are intractable, called neurofibrillary tangles. Most of the tau protein, which is a component of the microtubule structure, makes up these tangles. From one area of the nerve cell to another, the microtubule facilitates the movement of nutrients and other vital molecules.
These tangles interfere with the transport mechanism of the cell, impairing synaptic transmission between neurons. New research reveals that aberrant tau and beta-amyloid proteins, along with a number of other factors, may play a complex role in the development of the brain abnormalities associated with Alzheimer's disease.
A decrease in concentration and function of acetylcholine (ACh), a neurotransmitter crucial for processing memory and learning, is observed in Alzheimer's disease patients.
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