Transcript Cognitive Decline: The Aging Human Brain

• What is Aging?
• Alzheimer’s Disease
• Parkinson’s Disease
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Denoted by the following:
 Declining ability to respond to stress.
 Increased homeostatic imbalance.
 Increased risk of aging-associated diseases.
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Death is the ultimate consequence of aging.
 Gompertz-Makeham Law of Mortality▪ Mortality rate rises rapidly with age.
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Organismal Senescence:
 Process in which normal diploid cells loose
their ability to divide.
 Shortened telomeres (ends of chromosomes).
 Causes cellular apoptosis .
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Hayflick Limit:
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Human- 50 cell divisions in vitro
Lobster- unlimited
Each mitosis shortens the telomeres on the DNA of the cell.
Telomere shortening in humans eventually blocks cell division and
correlates with aging.
 This mechanism prevents genomic instability and the development of
cancer. (Carnosine can increase the Hayflick limit in humans.)
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Why do our cells do this?
 Prevents tumor cell proliferation.
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Fountain of Youth:
 Why is the cure for cancer much more
important than treating cancer?
 Polyploidy cells allow for cellular immortality.
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Henrietta Lacks (HELA)
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Changes:
 Brain and spinal cord lose nerve cells and weight.
 Nerve cells transmit messages more slowly.
 Waste products collect in brain tissue as nerve cells break down
creating abnormal structures called plaques and tangles.
 Reduced or even lost reflexes and sensation.
 Slowing of thought, memory.
 Senility is not a factor in aging,
it is a factor caused by illness of the brain.
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Form of dementia that gradually gets worse over time.
Affects memory, thinking, and behavior.
Includes problems with language, decision-making,
judgment, and personality.
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Risk Factors:
 Age (not a part of normal aging).
 Close blood relatives.
 Certain combination of genes for proteins that appear to
be abnormal in Alzheimer's.
 Longstanding high blood
pressure.
 History of head trauma.
 Female gender.
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Two Types:
 Early Onset-Symptoms before age 60 and much less common.
 Late Onset-Symptoms after age 60 and much more common.
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Diagnosis:
 The only way to know for certain that someone has AD is to
examine a sample of their brain tissue after death.
 Neurofibrillary tangles-twisted fragments of protein within
nerve cells that clog up the cell.
 Neuritic plaques-abnormal clusters of dead and dying nerve
cells.
 Senile plaques-areas where products of dying nerve cells have
accumulated around protein.
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When nerve cells (neurons) are destroyed, there is a
decrease in the chemicals that help nerve cells send
messages to one another (called neurotransmitters).
As a result, areas of the brain that normally work together
become disconnected.
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Treatment:
 There is no cure for AD.
 The goals in treating :
▪ Slow the progression of the disease
▪ Manage behavior problems, confusion, sleep problems,
and agitation
▪ Modify the home environment
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Medication:
 Donepezil (Aricept), rivastigmine (Exelon), and
galantamine (Razadyne, formerly called Reminyl) affect
the level of a chemical in the brain called acetylcholine.
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Part of the brain that controls muscle movement (midbrain and
substantia nigra involved).
Dopamine producing neurons.
Characterized by the accumulation of alpha-synuclein protein forming
inclusions called Lewy bodies.
 This can only be demonstrated in autopsy.
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Symptoms:
 Trembling of hands, arms, legs, jaw and face
 Stiffness of the arms, legs and trunk
 Slowness of movement
 Poor balance and coordination
 Symptoms will continue to
get much worse.
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Begins around age 60.
More common in men than in women.
There is no cure for Parkinson's disease.
Increased risk of PD in those living in rural environments and
those exposed to pesticides.
Reduced risk in smokers.
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Treatment:
 Levodopa, dopamine agonists, and MAO-B Inhibitors
(reduce symptoms).
 As the disease advances the use of medication produces
motor symptoms known as dyskinesias.