Lecture 12 Flashcards
hypoxia
mental impairment due to oxygen deprivation
lack of social stimulation and love
lasting inability to show love
consequences can be more severe than physical deprivation (world war two english school children)
fetal alcohol exposure basic stats and what it causes
1/1000 births, effects range from range from less severe fetal alcohol effects (FAE) to very severe fatal alcohol syndrome (FAS)
includes facial deformities, impaired cognitive functions (learning, memory, attention, and mental retardation)and motor impairments
fetal alcohol exposure disruptions
interferes with growth factors that regulate cell division (neurogenesis)
disruption of radial glial (neuronal migration)
disruption of neurotransmitter systems (NMDA glutemate receptor) which is important for stabilizing synapses during development
disruption of glucose transport proteins
disruption of cell adhesion molecules, which are important for synaptic connectivity
FAE and the cerebellum
massive loss of purkinje cells
poor coordination, motor skill deficits
depends on dose, pattern (e.g. binge drinking) and timing of exposure
later interventions at best only partially successful
fragile X syndrome cause, stats, and failure to what
caused by breaking or malfunction of the end of the X chromosome as a result of too many repeats (CGG should be repeated up to 50 times, with the disease, it’s as high as 200 times)
most common form inherited mental retardation
twice as common in males
can cause autism
results in failure to manufacture a particular protein (FMRP) and in results in a deficit in losing synapses
show enlarged areas with too many cells
autism spectrum disorder
S,V,R,B
wide range of individual variability, but includes deficits in: social interaction (primary deficit), verbal and nonverbal communication, repetitive behaviors or interests (modeling) some have cognitive deficits behavioral abnormalities (failure to make eye contact)
child disintegrative disorder CDD
some can appear to show normal development for months even up to 3 years followed by severe decline in functioning (less of language, social withdrawals)
social symptoms in ASD
SB, R, PP, SC, TM
do not exhibit typically early social behavior (gazing at people, turning towards voices, smiling)
may appear indifferent to other people, reluctant to cuddle or hug family members
may arrange toys rather than pretend play
or may engage in parallel play
have difficulty in interpreting social cues (facial expression, wink, tone of voice)
impaired theory of mind= interfering another’s thoughts
ASD and face processing
subjects with ASD show reduced activation when processing familiar faces
unaffected people look at mouth and eyes, ASD focus on movement and not look at mouth or eyes
can’t really identify the emotions on face
ASD and the brain
high local connectivity and low long range connectivity
means they are good at focusing on one task but not at switching, poor long range connectivity that lead to impaired integration of info
down syndrome and what they have a greater risk of
trisomy (3 copies) 21 ( chromosome)
over produces amyloid precursor protein APP
a symptom of Alzheimer disease is production of beta amyloid which comes from APP
people with down syndrome have a greatly increased risk of early onset alzheimers (in 30’s)
progressions of Alzheimer’s
mild cognitive impairment forgetfulness confusion restlessness alternating with lethargy errors in judgement hostility major motor impairment
microscopic observations of Alzheimer’s
senile plaques
neurofibrillary tangles
decrease in oligodendrocytes (which make myelin)
Result: neurons in the cholinergic pathway die which affects hippocampus (center of memory)
senile plaques and Alzheimer’s
Senile plaques consist mostly of beta amyloid proteins (used in NMDA receptor) accumulates around axons and dendrites to prevent synaptic transmission
neurofibrillary tangles and Alzheimer’s
excess build up of beta amyloid protein messes up tau proteins, over phosphorylated or activated too long causes neurofibrillary tangles to tangle up with themselves
what happens when the beta amyloid is cut wrong
mutation occurs when the amyloid precursor protein is cut too long, instead of 40 amino acids it is 42-43. this causes it to be too long so when embedded in the membrane causes holes and leads to cell death
primary cause of Alzheimer’s
is the build up of bad beta amyloid proteins
