by Joerg Bauer 15 years ago
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As shows Schizophrenia evenif identical twin has it there is onlya 50% chance
So there is an environmentalside to it
Brain Scans(can only be usedto exclude other conditions)
CT
Pet scan
MRI
fMRI
Cognitive Tests
i.e. Memory Tests
Behavioural assessment
Skilled Doctors
i.e. microscopy
Lesion in the Hippocampus
other aren't
Genes: inheriting a certain allele of a protein apolipo protein e
Age is highest risk factor
behaviour factors are under our control (healty life style)
clinical depression
smoking
arthereosklerosis
hypertension
diabetes
elevated cholesterol and obesity
head injury (boxers)
However only 50% of monocygotic twinsdevelope schizophrenia
However only < 10 percent of the occurrance can be acounted for gene defects
Raphe Nuclei
Regulation of mood(serotonergic projections to the cortex)
depression
Lymbic structures
Amygdala
the appreciation of theemotional significancof sth. in a normal way is lost
fear
mood changes
abnormal social behaviour
Hippocampus (old cortex) and Entorhinal cortex (neocorte)
learning and memory- short term memoryin particular
are among thefirst areas to degenerate
-->loss of short term memory
Neocortex
loss in highest order assotiation areas
primar areas remain intact(propriocepton; smell, taste touch, vision, hearing)
Prefrontal cortex
ability to plan andreason is lost
-->hence confusion
Abnormal chnange in extracellular space
NeurofibrilaryTangles
abnormal depositions (filament) in Neurons
Intracellular: Abnormal changesin Neurons
Plaques
Abnormal extracellular depositsof (normal) Beta-Amyloid Protein surrounded by abnormal neuronal processes and glial cellswho try to get rid of it
Gradual loss of physiological (bodily)functions
Leading to death
Mean time from diagnosis to death= 7 years
Heamorrhage in the brain
because of depostion ofamyloid in blood vessels which makes them rupture
loss of cog funct
Language break down
Memory Loss
Loss of sense of self:individuals forget who they are
Loss of episodic memoryin Hippocampus
Long term memory loss
late stage because ltm is widely distributed
Emotional problems
Mood swings
irritability
agression
significant Losss of cog. function
loss of higher ordre cog func. like inabilty to understand jokes
significant memoryloss
Depression
Decreased initiative(loss of interest in hobbiesor personal hygiene)
Faulty judgement
Deficits in attention
Loss of Short TermMemory (Can't rememberrecently learned things)
Animal model: An animal model using mice with a mutation in the gene coding for APP can show this
show tangles and plaques
show Impairment
Impairments in spatial tasks
shows age dependet (at 10 month) impairment in learning
... result of boht a) and b) is a toxic form of of Amyloid called beta amyloid
released in extracellular space forming aggregates called plaques which are toxic
b) Mutations involved in the processing of APP (enzymes)so that APP ins inappropriately cleaved
a) Gene that codes for amyloid precursor protein (APP) can have a numver of mutations
for the rest: cause unknown!
45% of People over 85
Intracellular Tangles (Hyperphosphorylated tau protein)
Extracellular Plaques (Beta Amyloid Protein)
no loss of primary areas
A specific type of progressive dementia (there are other dementias)
Characterized by neuron loss in specific areas
Significan neurons loss in the CNS - neurons are dying