MODULE SUPPLEMENT: NEUROLOGICAL SYSTEM
Incidence of Cognitive Impairment
Why does the incidence of cognitive
impairment increase with age?
Changes in neurons, including the alterations that occur in dendritic
density, synapses, and neurotransmitters alters the connectivity of the
central nervous system while overall cell loss and decreased blood flow
and metabolism point to lower reserve capacity. But by themselves, do these
necessarily lead to the types of loses seen in dementing conditions?
Here we need to consider additional changes that disrupt cellular function
and communication and consider what underlies these changes. A major focus
of research has been on neurofibrillary tangles and senile plaques, both
of which are found extensively in Alzheimer's disease.
Neurofibrillary tangles are structures that are found within
the neuronal cytoplasm and are composed of masses of silver staining fibers,
each consisting of a pair of filaments that are wound around each other.
(See OUHSC Alzheimer's Disease--Neurofibrillary Tangles for pictures
of various stained tangles--Note: This link will open in a new browser window which you can close to return here.)
While NFT are found it older persons who are not demented - in fact,
in some cases the early signs of these tangles can be found in relatively
young individuals (Braak, et al., 1999) - they are especially prominent
in persons with Alzheimer's disease and especially in areas such as the
hippocampus and amygdala, both of which are involved in memory. These indicate
disruption of the intracellular microtubules that are critical for normal
neuronal function.
Senile plaques are extraneuronal substances that are composed
of degenerating neuronal processes, reactive astrocytes, and amyloid (central
core). (See http://www.ahaf.org/alzdis/about/AmyloidPlaques.htm
for pictures of
senile plaques and their development--Note: This link will open in a new browser window which you can close to return here). Like NFTs, these can be found in
persons who are not demented, but are especially prominent in Alzheimer's
disease. Thus, disruption in the normal metabolism of amyloid has been a
major focus of research.
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