Alzheimer’s Disease

What is Alzheimer’s Disease? • It is the most common form of dementia. • Describe by a German physician, Alois Alzheimer. • Frau Auguste, first one diagnosed.

Dementia  a syndrome of intellectual deterioration severe enough to interfere with occupational or social performance.  disturbances in memory, language use, perception and motor skills, and may interrupt the ability to learn necessary skills, solve problems, think abstractly and make judgments.

Anatomy of the Brain
Cerebrum - largest and uppermost division of the brain.
contains Limbic System contains frontal, parietal, temporal, and occipital lobes.

Limbic System- “emotional brain” – mediate emotions, learning and memory – consists of fornix, hippocampus, cingulate gyrus, amygdala, parahippocampal gyrus, and parts of the thalamus.

Amygdala • Limbic structure involved in many brain functions, including emotion, learning and memory. Cingulate gyrus • Plays a role in processing conscious emotional experience.

Hippocampus • Plays a significant role in the formation of long- term memory. Cortex • Capable of storing and retrieving both short and long-term memory.

What is the Cause?
 There is no known and proven to be the primary cause of AD but several studies shows the involvement of plaques and tangles in neurons.

1. Amyloid Plaques
 deposits of beta-amyloid protein that accumulate in the spaces between nerve cells. Amyloid Beta protein - protein fragments that the body produces normally. - a fragment of a larger protein called Amyloid Precursor protein (APP).

2. Neurofibrillary Tangles
 deposits of protein tau that accumulate inside of nerve cells. Tau protein - forms part of structure called microtubules in the axon of neuron. - protein that stabilizes the microtubules when phosphorylated.

 Scientists are still studying how plaques and tangles are related to Alzheimer’s Disease. One theory is that they block nerve cells ability to communicate with each other, making it difficult for neurons to survive.

Common Risk Factors  Age - The greatest known risk factor. Most individuals with the illness are 65 years and older.

 Genetic - majority of AD cases are lateonset and shows no inheritance. However, in some families, clusters of cases are seen. - A gene Apolipoprotein E appears to be a risk factor for the lateonset of AD.

- Familial Alzheimer’s Disease or earl y- on set disease is an inherited rare form of the disease. - It is cause by one of the gene mutations on chromosome 1, 14, and 21. - mutation of APP gene on chromosome 21.

Symptoms and Stages Cognitive Symptoms 2. Language difficulty 3. Memory loss 4. Poor judgement 5. Problems with abstract thinking

Behavioral Symptoms 2. Sleep disturbances 3. Hallucinations 4. Mood swings 5. Changes in personality

Stages of

Al zheim er ’s Di sease

3. First Stage (mild) • can last from 2 to 4 years • Exhibit minor memory loss and mood swings and are slow to react and learn.

2. Second Stage (moderate) • This is generally the longest stage and can last 2 to 10 years. • Can still perform task but needs assistance with more complicated activities. • Clearly becoming disabled

3. Third Stage (severe) • This stage may last 1 to 3 years. • People may lose the ability to feed themselves, speak, recognize people, and control bodily functions. • Memory worsens

 Diagnosis of Alzheimer’s Disease are based on: 2. Mental and behavioral symptoms 3. Physical examination 4. Neuropsychological tests

Mental and Behavioral Symptoms
• Physician will normally take a history of mental and behavioral symptoms, using information provided by patient and the family.

Physical Examination
• Physical examination will be performed to help identify other potential causes of dementia • Includes blood tests, urinalysis, etc. • Magnetic Resonance Imaging (MRI) • Electroencephalogram

Neuropsychological Tests
• Identify behavioral and mental symptoms associated with brain injury or abnormal brain function  Many scientists are searching new ways to inexpensively and reliably diagnose AD earlier and with more accuracy.

• Common AD treatment
1) Acetylcholinesterase inhibitor - Slow the metabolic breakdown of acetylcholine and make more of this chemical available for communication between cells.

Brand Name Generic Name Side Effects Effective for

1. Razadyne galantamine

Nausea, vomiting, diarrhoea, weight loss Early to moderate AD Nausea, vomiting, diarrhoea, weight loss, weakening

2. Exelon 3. Aricept

rivastigmine donepezil

Early to moderate AD

Nausea, vomiting, Early, moderate, and diarrhoea, weight loss severe AD Possible liver damage, nausea, diarrhoea

4. Cognex


Early to moderate AD

2) Glutamate Antagonists
– – Namenda (memantine) is the only currently available drug that adjust the activity of glutamate Side effects are dizziness, confusion, headache, and constipation.

Parkinson’s Disease

What is Parkinson’s Disease?  It is a degenerative disease of CNS that often impairs the motor skills and speech and other functions.  Named after James Parkinson, a british physician who first describe PD in his paper published 1817 about “Shaking Palsy”

 In our brain, the substantia nigra which is a part of basal ganglia have this dopaminergic neurons that produces dopamine.  Dopamine is a neurotransmitter responsible for transmitting signals between the sustantia nigra and multiple brain regions.

 PD is characterized by progressive destruction of the nigrostriatal pathway, with subsequent reduction in striatal concentrations of dopamine.

 The mechanism by which the brain cells in PD are lost may consist of an abnormal accumulation of the protein alphasynuclein.

 Alpha- synuclein accumulation forms proteinaceous cytoplasmic inclusions called Lewy Bodies.

While it is still not known what causes PD, there are studies that have found some environmental and genetic link to the disease.

Possible Causes
- Recent development in gene research has found that genetic influence plays a role in Parkinson’s Disease. - 3 genes are identified that believed to contribute to the disease. This include alpha-synuclein, parkin, and ubiquitin carboxyl- terminal hydrolase.

ALPHA- SYNUCLEIN GENE • Located on chromosome 4 • Has been found to be associated with dementia in PD patients. • The mutations have also been associated with the young onset form of PD.


• Mutations in this gene have also been found to cause abnormal protein processing, where proteins should be degraded. When the gene is mutated, abnormal processing results in adverse cell reactions, which eventually lead to cell death.

PARKIN GENE • Parkin gene creates a protein also called parkin, helps breakdown defective proteins inside brain cells. When the parkin gene is altered, this function is impaired. It is hypothesized that the accumulation of defective proteins contributes to death of neurons.

ENVIRONMENTAL  TOXINS • There are number of toxins that can cause Parkinson symptoms in humans.

• 1-methyl-4-phenyl-1,2,3,6tetrahydropyridine or MPTP, found in some kinds of synthetic heroin. Its toxicity possibly comes from generation of reactive oxygen species.

• Excessive accumulation of iron, which are toxic to nerve cells. Iron and other transition metal are believed to bind to neuromelanin in the affected neurons of the substantia nigra. It generates reactive oxygen species.

• Free radicals of mitochondria. Free radicals are molecules that damage membranes, proteins, DNA. This damage is called oxidative stress. • Other suspected toxins are pesticides, viruses and substance that generates reactive oxygen species.

HEAD TRAUMA • Recent study found that those who have experienced a head injury are four times more likely to develop PD than those who have never suffered a head injury. • Rare event, PD incidence is slight.

Symptoms and Stages
Shaking (tremor) of the arms and legs initially on one side of the body while resting or walking. Stiffness (rigidity) when an arm, leg, or the neck is moved. The muscles remain constantly tensed and contracted, so the person feels stiff and weak.

Slowness of movement (bradykinesia), especially in starting and attempting to continue rapid repetitive movements. Poor balance, difficulty walking with shuffling of the feet. Fatigue Emotional changes such as depression

Decline in mental function over time Sleep disturbances Problems with swallowing, speech, bladder control and constipation Small, cramped handwriting Impaired sense of smell Visual hallucinations

Symptoms on one side of the body only Symptoms on both sides of the body. No impairment of balance. Balance impairment. Mild to moderate disease. Physically independent

Severe disability, but still able to walk or stand unassisted. Wheel chair- bound or bedridden unless assisted.

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