Neuro Flashcards
Pre clinical AD
-measurable brain changes without symptoms
-biomarkers: beta-amyloid shown on PET scan and cerebrospinal fluid(CSF), abnormal levels of tau protein
Early symptoms of AD
-language problems
-misplacing items
-getting lost on familiar routes
-personality changes
-losing interest in things
-difficulty preforming tasks that take some thought
Worsening AD symptoms
-forgetting current events
-change in sleep patterns
-difficulty reading ot writing
-hallucinations
-delusions
Severe AD symptoms
-unable to understand language
-will not recognize family members
-can not preform basic activities
Sporatic AD
-most common form
APOE
transports cholesterol and other fats through the body
-may be involved in structure and function of the fatty membrane surrounding brain
–APOE-e4 associate with AD
APOE forms
-APOE-e2: least common
-APOE-e4: more common
-APOE-e3: most common
Chronic Traumatic Encephalopathy (CTE)
0mostly in athletes
0many also have AB plaques and tangles in astrocyte and neurons
-Impulsive, depressive symptoms, apathy, anxiety, hopelessness, violence, suicide
Neurodegeneration in AD
-disruption of calcium regulation/homeostasis
-damage mitochondria
-chronic activation of immune response
-impaired protein clearance/protein turnover
-synaptic dysfunction
-tau phosphorylation leading to NFT formation
-All of the above occur naturally with increasing age
Macroautophagy
-TORC1 inhibits autophagy
-AMPK prompts this process
-constant battle between the two
-in AD, we see increase of TORC1, which means that autophagy has been reduced
Intracellular accumulation of AB
-APP localizes to the plasma proteins
-APP turnover is mediated by endosomal internalization
-Autophagosomes/autolysosomes accumulate in neurons of AD brain
-Overexpression of mutant APP leads to AB peptides and/or other APP fragment accumulation in autophagic vesicles
