2. INTRODUCTION
Neurodegenerative disorder are characterized by progressive and
irreversible loss of neurons from specific regions of the brain.
Prototypical neurodegenerative diseases.
1. Parkinson's disease (PD)
2. Huntington's disease (HD)
-In both there is loss of neurons from structures of the basal
ganglia results abnormalities in the control of movement.
3. Alzheimer's disease (AD)
-Where the loss of hippocampal and cortical neurons leads to
impairment of memory and cognitive ability.
4. Amyotrophic lateral sclerosis (ALS)
-Where muscular weakness results from the degeneration of
spinal, bulbar, and cortical motor neurons.
Rang and Dale’s Pharmacology, 6th ed.2
3. What is Alzheimer’s disease (AD)?
Alzheimer’s disease is an irreversible,
progressive brain disease that slowly destroys
memory and thinking skills.
It is the most common cause of dementia.
Goodman & Gilman's The Pharmacologic Basis of Therapeutics - 11th Ed. (2006)3
4. HISTORY
In the year 1906 a German physician Dr. Alois
Alzheimer, specifically identified a collection of brain
cell abnormalities as a disease.
Alzheimer had a patient named Auguste D in her fifties
who suffered from mental illness But when she died in
1906.
Inside the nerve cells he observed twisted bands of
fibers (neurofibrillary tangles).
www.google.com4
5. 5
Inside the Human Brain
To understand Alzheimer’s disease,
it’s important to know a bit about
the brain…
• Adult weight: about 3 pounds
• Adult size:
a medium cauliflower
• Number of neurons:
100,000,000,000 (100 billion)
• Number of synapses
(the gap between neurons):
100,000,000,000,000
(100 trillion)
8. PATHOPHYSIOLOGY
Alzheimer's disease is associated with brain shrinkage and
localised loss of neurons, mainly in the hippocampus and basal
forebrain. The loss of cholinergic neurons in the hippocampus
and frontal cortex is a feature of the disease.
Two microscopic features are characteristic of the disease,
namely extracellular amyloid plaques, which are dense
deposits of protein and cellular material that accumulate
outside and around nerve cells of β-amyloid protein (known
as Aβ), and intraneuronal neurofibrillary tangles, which are
twisted fibers that build up inside the nerve cell of protein
(Tau).
8
9. DUE TO THE ETIOLOGICAL FACTORS
CHANGES OCCUR IN THE PROTIENS OF THE NERVE
CELLS OF THE CEREBRAL CORTEX
ACCUMULATION OF NEUROFIBRILLARY TANGLES
AND PLAQUES
GRANULO VASCULAR DEGENERATION
LOSS OF CHOLINERGIC NERVE CELLS
LOSS OF MEMORY, FUNCTION AND COGNITION
9
11. 11
Beta-amyloid Plaques
Amyloid precursor protein (APP) is
the precursor to amyloid plaque.
1.APP sticks through the neuron
membrane.
2. Enzymes cut the APP into
fragments of protein, including
beta-amyloid.
3. Beta-amyloid fragments come
together in clumps to form plaques.
In AD, many of these clumps form,
disrupting the work of neurons. This
affects the hippocampus and other
areas of the cerebral cortex.
12. Neurons have an internal support structure partly made up of
microtubules. A protein called tau helps stabilize microtubules.
In AD, tau changes, causing microtubules to collapse, and tau
proteins clump together to form neurofibrillary tangles12
13. SIGNS
Ten warning signs of Alzheimer's disease
1) Memory loss
2) Difficulty to performing familiar tasks
3) Problems with language
4) Disorientation to time and place
5) Poor or decreased judgment
6) Problems with abstract thinking
7) Misplacing things
8) Changes in mood or behavior
9) Changes in personality
10) Loss of initiative
13
14. SYMPTOMS
1. Confusion
2. disturbances in short-term memory
3. problems with attention and spatial orientation
4. personality changes
5. language difficulties
6. unexplained mood swings
14