What is Aging? Alzheimer’s Disease Parkinson’s Disease

 Denoted by the following:  Declining ability to respond to stress.  Increased homeostatic imbalance.  Increased risk of aging-associated diseases.  Death is the ultimate consequence of aging.  Gompertz-Makeham Law of Mortality- ▪ Mortality rate rises rapidly with age.

 Organismal Senescence:  Process in which normal diploid cells loose their ability to divide.  Shortened telomeres (ends of chromosomes).  Causes cellular apoptosis.  Hayflick Limit:  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.)

 Why do our cells do this?  Prevents tumor cell proliferation.  Fountain of Youth:  Why is the cure for cancer much more important than treating cancer?  Polyploidy cells allow for cellular immortality.

 Henrietta Lacks (HELA)

 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.

 Form of dementia that gradually gets worse over time.  Affects memory, thinking, and behavior.  Includes problems with language, decision-making, judgment, and personality.

 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.

 Two Types:  Early Onset-Symptoms before age 60 and much less common.  Late Onset-Symptoms after age 60 and much more common.  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.

 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.

 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  Medication:  Donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne, formerly called Reminyl) affect the level of a chemical in the brain called acetylcholine.

 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.

 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.

 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.

 Treatment:  Levodopa, dopamine agonists, and MAO-B Inhibitors (reduce symptoms).  As the disease advances the use of medication produces motor symptoms known as dyskinesias.