Alzheimer’s Disease (AD) By Jenny Piciw

Characteristics Adult on-set dementia Memory loss Confusion Poor judgment Decrease in communication Agitation Hallucinations Seizures Cortex shribels up  thinking, planning, memory Hippocampus  key role in formation of new memories Ventricles  fluid filled spaces  become larger

Factors Head Trauma Heart-head connection Management of other health conditions Healthy Aging Head-heart connection  alztiemer’s due to damage of the brain and it has been proven that people how have had strokes and heart attacks have an increased risk of alzheimer’s diesease  this is because of decreased blood flow to the brain which does not allow for proper function Other health conditions  diabetes

Link with Genetics Risk Genes Deterministic Genes Direct cause of AD Increase probability Not a direct cause of AD APOE-e4 Deterministic Genes Direct cause of AD Inheritance  AD Autosomal Dominant Alzheimer’s Disease (ADAD) Early onset  typically between 30-60 No widespread cause APP PS-1 PS-2

Genetic Trends of ADAD Affected individuals  affected parents Siblings  50% chance of also inheriting Occasionally identified in second degree relative Could also be caused by de nova mutation Siblings  chances of inheriting are small

APOE-e4  Apolipoprotein E-e4 1993  first discovered  greatest impact Mutant form of APOE Normal combines lipids to form lipoproteins 1 copy  slightly increased risk 2 copies  higher risk Factor of 20-25% of cases Earlier onset

Amyloid Precursor Protein (APP) 1987 50+ mutations ADAD Lead to increased amyloid β peptide  amyloid plaques Type 1 (early onset) 10-15% of ADAD cases

Presenilin-1 (PS-1) 1992 Normal  development of brain+ spinal cord  activates genes  cell growth and maturation 150+ mutations  amyloid plaques  kills neurons 30-70% of cases of ADAD Presenilin-1 is believed to work with other enzymes to cut APP into peptides  soluble APP  growth-promoting properties  nueron formation before and after birth

Presenilin-2 (PS-2) 1993 Normal processes proteins  chemical signals from cell membrane to nucleus 11+ mutations  disrupt APP processing ˂ 5% of cases of ADAD 95% penetrance Presenilin-2 is believed to work with other enzymes to cut APP into peptides  soluble APP  growth-promoting properties  nueron formation before and after birth

Diagnosis Biomarkers  can accurately determine the presence or absence of a disease Brain Imaging  MRI or PET Proteins present in the fluid around the brain Current methods : Magnetic resonance imaging Positron emmission tomography

Treatment Do not cure AD Help with cognitive and behavioral symptoms Cholinesterase Inhibitors Mematine Vitamin E  aricept, exelon, razadyne, cognex Prevent break down of acetycholine  messanger important for learning and memory Namenda Regulates activity of glutamate  involved in learning and memory Help with memory loss, confusion and reasoning ability Vitamin E  antioxidant  protects brain cells and the body tissue from chemical wear and tear  high doses delay loss of ability to carry out daily activities

Things you should remember: AD is a disease that impairs cognitive function Genetic factors can put one at risk or can be deterministic One can be at increased risk if they have the following: Brain trauma Heart Attack Uncontrolled diabetes Are generally not healthy Carry one or more copies of the APOE-e4 gene If a person carries a mutation in any of the following it will lead to AD APP PS-1 PS-2 Amypliod B

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