 ALZHEIMER'S DISEASE RELATED TO DEMENTIAS

The pathogenesis of AD is uncertain but the disease includes specific neuropathologic and biochemical
changes that interfere with neurotransmission. These changes consist of neurofibrillary tangles (tangled
masses of nonfunctioning neurons) and senile or neuritic plaques (deposits of amyloid protein, part of a
larger protein called amyloid precursor protein in the brain) (see Fig. 11-5). The neuronal damage occurs
primarily in the cerebral cortex and results in decreased brain size. Similar changes are found in the
normal brain tissue of nonsymptomatic older adults, although to a lesser extent. Cells that use the
neurotransmitter acetylcholine are principally affected by AD. At the biochemical level, the enzyme
active in producing acetylcholine, which is specifically involved in memory processing, is decreased.

Scientists have been studying complex neurodegenerative diseases such as AD and have focused on two
key issues: whether a gene might influence a person’s overall risk of developing the disease, and
whether a gene might influence some particular aspect of a person’s risk, such as the age at which the
disease begins (age at onset). There are genetic differences in early- and late-onset forms of AD (Sherva
& Kowall, 2015). Researchers are investigating what predisposes people to develop the plaques and
neurofibrillary tangles that can be seen at autopsy in the brains of patients with AD. Understanding the
complex ways in which aging as well as genetic and nongenetic factors affect brain cells over time,
eventually leading to AD, continues to increase.

 PARKINSON’S DISEASE
 CREUTZFELDT-JAKOB DISEASE
 HUNTINGTON’S DISEASE
 MULTIPLE SCLEROSIS
 PARALYTIC DISEASES
 AMYOTROPHIC LATERAL SCLEROSIS