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166 Cards in this Set
- Front
- Back
where in the brain is language primarily
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left cerebral cortex
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which hemisphere is capable of speech
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left hemisphere
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does right brain have some understanding of language
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YES
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major language regions in the left brain
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broca's area, motor cotex, angular gyrus, wernicke's area, auditory cortex
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what is aphasia
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loss of ability to produce and/or to comprehend language
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what is wernicke's aphasia
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fluent aphasia=patients easily generate words, but the statements have little meaning
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what are paraphasic errors
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when patients substitute incorrect sounds or words.
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what is broca's aphasia
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motor or nonfluent aphasia= patients have difficulty generating words
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what is aggramatism
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patients don't use function words (articles, pronouns, conjuctions)
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what is the first stage of language processing
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frequency and temporal analysis carried out bilaterally in auditory cortex followed by phonological processing (extracting phonemes)
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two streams in language processing
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1. ventral stream
2. dorsal stream |
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ventral stream
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maps sensory information onto "lexical conceptual representations"
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dorsal stream
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maps sensory information onto "articulatory motor representations"
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what is one problem associated with learning to speak a language
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spoken language doesn't reliably indicate breaks between words with a pause
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which properties of syllables do humans identify and use
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statistical properties
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what is attention
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a neural process by which you enhance your perception of certain stimuli relative to other stimuli in the environment
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what is bottom-up attention
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when the object “grabs” your attention without conscious knowledge of the stimulus. The stimulus is more salient than the background.
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what is top-down attention
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you consciously look for a specific object
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steps in change blindness
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1. visual transients produced by changes in color, shape,orientation that draw your attention to the location of the change
2. visual memory of what was at the site of the change so that you can identify what changed |
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what does attention enhance
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detection of stimuli at site of attention
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what does attention reduce
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detection of stimuli away from site of attention
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what might the parietal lobe be involved in
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disengaging visual attention
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4 steps of shifting attention
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1. disengage from present location
2. move your attention to the new location 3. engage your attention at the new location 4. inhibit the previous site of attention |
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neglect syndrome
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damage to the right parietal lobe disrupts visual attention to the left side of the visual space
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what does the parietal lobe participate in
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visual attention, in particular shifting visual attention
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Darwin's analysis regarding emotion
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1. cross-species similarities in the expression of emotion
2. there were a limited set of fundamental emotions |
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james lange's theory of emotion
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ANS changes precede and produce emotions. We experience emotion as a consequence of autonomic activity
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cannon-bard theory of emotion
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the stimulus activates the thalamus which distributed the inputs to the cortex to create emotion and autonomic changes simultaneously. the autonomic changes are independent of emotion.
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problems with james-lange theory
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-emotions can be experienced even if no sense of physiological response is present
-fearful & angry states have similar autonomic responses, how do different emotions arise from similar physiological states? |
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problems with canon-bard theory
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-emotions are less intense with the brain disconnected from the viscera
-artificial manipulations of autonomic activity can induce emotions |
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zajonc theory of emotion and facial efference
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changes in venous blood flow created by patterns of facial muscle contractions produces small changes in brain temperature that alters mood
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describe the two stream circuit of emotion starting with the "thought stream" thalamus
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->sensory cortex ->cingulate gyrus produced perception, thought, and memory
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describe the two stream circuit of emotion starting with the "feeling stream" thalamus
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->mammillary bodies (hypothalamus)-> anterior thalamus -> cingulate cortex evoked the body's physiological response.
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what do emotions result from
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cingulate cortex activity
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what can emotions be evoked from
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sensory stimuli (thought stream) or physiological responses (feeling stream)
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what neural system did MacLean outline
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the limbic system= emotion arises by integrating external sensations with information from the body.
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what parts of brain play important roles in emotion
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-ventromedial prefrontal cortex/orbital frontal
-amygdala -anterior cingulate cortex -nucleus acumbens -vental pallidum (basal ganglia) -hypothalamus/basal forebrain |
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what did Domasio and colleagues hypothesize
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that PFC creates "somatic markers" that link ANS activity to emotionally significant previous events, the somatic marker hypothesis
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what cant PFC lesion patients do
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identify long-term negative or positive consequences
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effect of frontal lobotomies
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disconnect the frontal and cingulate cortex in individuals with severe psychosis, blocking "too much" emotion
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amygdala
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"almond shaped" nucleus in the anterior end of the temporal lobe with several subdivisions- involved in fear
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evidence required to show that amygdala is involved in fear conditioning
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1. lesion of the amygdala b4 learning should prevent acquisition of fear conditioning
2. blocking cellular changes in the amygdala necessary to convert short-term to a long term memories should prevent long-term conditioned fear 3. the amygdala should alter its activity with fear conditioning |
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does memory for emotional stimuli differ between sexes
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YES
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explain women's superior memory for emotional pictures
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better integration of brain processes associated with emotional experience into memory
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what is the insula
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neural center for disgust
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what receives emotional info for further evaluation
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1. rostral anterior cingulate cortex
2. dorsal anterior cingulate cortex 3. dorsomedial prefrontal cortex 4. ventromedial prefrontal cortex |
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what do raCC and vmPFC do
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-gate info flow into conscious awareness
-provide excitatory and inhibitory feedback to core limbic structures |
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what is arousal a measure of
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excitement level
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what is valence a measure of
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positivity
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part of brain associated with positive arousal
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nucleus accumbens
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part of brain associated with negative arousal
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amygdala
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where does nucleus accumbens receive dopamine input from
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ventral tegmental area (VTA)
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in who does activation of nucleus accumbens occur
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ppl who report experiencing pleasure
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what do humorous stimuli inc
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blood flow in many brain regions including nucleus accumbens
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what does amphetamine cause
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release of dopamine from dopamine terminals
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what is nucleus accumbens
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rostral striatum region in humans where the caudate and putamen and not divided by the internal capsule
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how much do the primary sensory and primary motor area account for
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20% of the neocortex
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association cortex
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remaining 80% of neocortex which is involved in further perceptual processing of sensory info, in motor planning, and in cognition
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cognition
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collective term for the complex functions of the brain having to do with language, thought, and the construction perceptions
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what does the neurochemical basis of mental illness typically involve
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norepinephrine, dopamine, serotonin
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cartesian dualism
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body and mind were considered separate entities- disorders of the body has a physical cause and were province of medicine but disorders of the mind had a spiritual or moral basis and were the province of religion
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Freud's influence on mental illness views
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mental illness arose from conflict between conscious and unconscious aspects of the psyche (mind)
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Freud's treatment for mental illness
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helping patients uncover incidents, usually from childhood that were suppressed from consciousness and hidden in the unconscious mind.
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how did psychopharmacology treatment of mental illness start
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with the chance discovery of antipsychotic action of chloropromazine (1952)
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what does biological psychiatry attempt to do
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establish the underlying neurochemical basis for mental illness
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anxiety disorders
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inappropriate expression of fear that is disabling
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stressor
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threatening stimulus
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what is the stress response characterized by
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-avoidance behaviors
-elevated arousal and vigilance -activation of sympathetic division of the ANS -release of cortisol (a glucocorticoid hormone) from the adrenal glands |
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normal response to stress
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hypothalamic-pituitary-adrenal (HPA) axis:
-release of cortisol from adrenal glands is triggered by ACTH -ACTH is released by the anterior pituitary gland under control of parvocellular neurosecretory neurons located in the paraventricular nucleus of the hypothalamus -parvocellular hypothalamic neurons release CRH into the blood of the portal circulation |
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what causes CRH (corticotropin releasing hormone) release
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neocortex & thalamus send sensory info that increases activity in the amygdala, which in turn activates the hypothalamus and stimulates CRH release
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where has inappropriate activation of the amygdala by non-threatening stimuli been implicated
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anxiety disorders
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effect of cortisol binding to glucocorticoid receptors on hippocampal neurons
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enhances their activity, inhibits CRH release from hypothalamic neurosecretory neurons. (hypothalamus provides neg feedback regulation of HPA)
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effect of continuous exposure of hippocampus to cortisol during chronic stress
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-reduces the number of dendrites of hippocampal neurons
-neuronal death in hippocampus -loss of inhibitory control of HPA axis by the hippocampus, inducing a vicious cycle of runaway activation |
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what have anxiety disorders been linked to
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-hyperactivity of the amygdala
-reduced activity in the hippocampus |
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describe the regulation of HPA axis by the hippocampus
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prolonged elevation of cortisol -> loss of neurons in the hippocampus -> dec. inhibition of HPA axis by the hippocampus
-> enhanced release of cortisol from adrenal glands ->cycle restarts |
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treatments for anxiety disorders
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-psychotherapy
-anxiolytic drugs |
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psychotherapy mechanism
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may use the ability of the brain to alter synaptic efficacy based on experience to reduce the ability of non-threatening stimuli to activate the stress response
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anxiolytic drugs
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-benzodiazepines
-selective serotonin reuptake inhibitors -serotonin norepinephrine reuptake inhibitors |
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benzodiazepine action
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bind to GABA_A receptors and make them more responsive to GABA.
(presumably they act to suppress activity of stress circuits) |
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ethanol affect on GABA
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facilitates GABA actions
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where are neurons that release serotonin found, where do they project to
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in the raphe nuclei of the brain stem and project diffusely through the brain and spinal cord
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how does serotonin act
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via G-protein coupled receptors to modulate neuronal activity in many brain regions
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what is serotonin's action terminated by
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reuptake via serotonin transporters
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what is SSRIs therapeutic effect caused by
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some unknown adaptive changes in the brain to chronically elevated external serotonin
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one adaptive effect of SSRIs
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increase the number of glucocorticoid receptors in the hippocampus- this might enhance the feedback inhibition of the HPA axis by the hippocampus
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norepinephrine
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diffuse modulatory system that targets many brain regions
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where are the neurons that release norepinephrine found
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in the locus coeruleus in the brain stem
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what is norepinephrine's action terminated by
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reuptake via norepinephrine transporters
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effect of SNRIs
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inhibit both serotonin and norepinephrine transporters, prolonging the action of both neurotransmitters
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affective disorders
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disorders of emotional state or mood (affect)
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major depression
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severe depression lasting >2 weeks, often without obvious external cause and often accompanied by the feeling of losing control of one's emotional state
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major depression symptoms
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-lowered mood & dec interest
-loss of appetite -insomnia -fatigue -feelings of worthlessness & guilt -diminished concentration -recurrent thoughts of death |
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dysthymia
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milder form of depression but is chronic
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what is bipolar disorder characterized by
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repeated bouts of mania or hypomania, sometimes alternating with depression
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manic phase
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-abnormally elevated, expansive, or irritable mood (DIGFAST)
Distractibility Indiscretion Grandiosity Flight of ideas Activity increase Sleep deficit Talkativeness |
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hypomania
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similar to mania but doesn't severely impair social interactions or work performance (in fact creativity & performance can be greatly enhanced)
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monoamine hypothesis
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depression and mania are disruptions of one or both of these diffuse modulatory systems (catecholamine & serotonin)
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clues that led to monoamine hypothesis
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1. treatment of high bp with reserpine, which blocks loading of serotonin & catecholamines into synaptic vesicles, caused depression in 30% of patients
2. a drug for treating tuberculosis that inhibited MAO (enzyme that degrades catecholamines & serotonin) produced mood elevation 3. the antidepressant drug, imipramine, was found to block the reuptake of serotonin and norepinephrine |
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what is the diathesis-stress hypothesis of affective disorders
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predisposing factors interact with stress to produce depression
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evidence supporting diathesis-stress hypothesis
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-anxiety & depression coexist in patients, and anxiety is related to HPA axis
-in depression, pituitary & adrenal gland are enlarged -in depression, # CRH neurons in hypothalamus and expression of CRH inc. -blood cortisol & CRH concentration in CSF are elevated in depressed patients -elevated CRH is reduced by treatments that alleviate depression -delivery of CRH to the brain in animals produces behavioral effects similar to depression in humans -rats that receive lots of maternal care as pups have inc glucocorticoid receptors in hippocampus, reduced reduced CRH in hypothalamus, less anxiety -inc in glucocorticoid receptors in hippocampus is mediated by serotonin release -effect of experience on adult anxiety is restricted to postnatal critical period -in humans, childhood abuse & neglect increase risk for developing affective & anxiety disorders -dec. feedback inhibition of HPA axis may make brain more susceptible to depression & anxiety |
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treatments for affective disorders
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-electroconvulsive therapy
-tricyclic antidepressant drugs (block reuptake of NE & serotonin) -selective serotonin reuptake inhibitors -MAO inhibitors (block enzyme degradation of serotonin & norepinephrine) -lithium (treats bipolar disorder) |
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psychosis
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loss of contact with reality
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schizophrenia
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disruption of perception, thought, mood, movement, and loss of contact with reality
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percent of population schizophrenia affects
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1% of population
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what are positive symptoms
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occurence of abnormal thoughts and behaviors
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examples of positive symptoms of schizophrenia
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delusions, hallucinations, disorganized speech, catatonic behavior
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what are negative symptoms
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absence of normal responses
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examples of negative symptoms of schizophrenia
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reduced expression of emotion, poverty of speech, difficulty initiating goal-directed behavior, memory impairment
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describe familial nature of schizophrenia
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variations in a number of genes have been linked to increased susceptibility to schizophrenia
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can genetic background enhance vulernability to developmental/enrionmental factors that lead to schizo?
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YES
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gross changes in schizophrenic brains
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1. ventricles are enlarged in the brain of schizo identical twin-> consistent with a loss of brain tissue in schizo
2. reduced metabolic activity in frontal lobes of schizo. patient-> consistent with reduced activity or loss of neurons in the frontal lobes of schizo. |
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what do amphetamine addicts sometimes experience
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amphetamine psychosis, with symptoms similar to schizo.
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what does amphetamine cause
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massive dopamine release
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what are drugs that improve positive symptoms of schizo. called?
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neuroleptic drugs-> blockers of dopamine D2 receptors
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what might be involved in schizo.?
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dopamine projections from VTA to the frontal lobes
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effect of "typical" neuroleptics targeting D2 receptors in the striatum and the cortex
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common motor problems (extrapyramidal symptoms) in patients taking these neuroleptic drugs->distinct gait that resembles Parkinson's
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what is dyskinesia
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another common side effect of neuroleptic drugs
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what naturally occurring compounds alter perception & cognition, and can induce hallucinations
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-psilocybin, found in psilocybin mushrooms
-mescaline, in peyote cactus |
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what does the similarity of hallucinogens and serotonin suggest
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that the diffuse serotonin neuromodulatory system might be involved in some of the symptoms of schizophrenia
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what have "Atypical" neuroleptics been found to be more potent blockers of
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serotonin receptors
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what symptoms do atypical neuroleptics reduce
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negative symptoms
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what do atypical neuroleptics affect
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other neurotransmitter systems like norepinephrine, histamine, and ACh
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what is phencylidine
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non-competitive antagonist of NMDA receptors, and it blocks by occupying a site within the open pore
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what other NMDA receptor blockers that occupy same site on open pore as phencylidine
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ketamine and MK-801
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what do NMDA hypomorphs exhibit
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schizophrenia-like symptoms, such as repetitive movements and altered social interactions
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glutamate hypothesis of schizophrenia
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reduced NMDA receptor activity plays a role in schizophrenia
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what are deficits in cognition caused by brain damage
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-agnosias
-apraxias |
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global cognitive loss
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alzheimer's disease
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what does damage in perisylvian fissure in dominant hemisphere lead to
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severe aphasias
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right hemisphere damage
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subtle deficits of language, humor or irony
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agnosia
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inability to identify objects based on sensory info, even though the primary sensory cortical areas are intact
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what do specific types of agnosia typically result from
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lesions in parietal or temporal lobe, in areas near the primary sensory cortex for the major sense
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what is tactile agnosia where patient has normal sense of touch in hands but cant identify object in hands
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astereognosis
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what's alexia
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-visual agnosia, which results from lesions of angular gyrus
-patients can can't recognize written words |
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prosopagnosia
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visual agnosia where patients are unable to recognize familiar faces
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apraxia
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difficulty in programming complex series of movements, without paralysis, sensory deficits, or problems performing simple tasks
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where are lesions responsible for apraxia
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in parietal and temporal areas
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different forms of apraxia
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-ideational apraxia
-ideomotor apraxia -limb-kinetic apraxia -orofacial apraxia -verbal or speech apraxia |
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what do lesions in supramarginal gyrus produce
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conduction aphasia and a form of apraxia in which patients cant follow verbal commands to carry out motor actions (similar to ideomotor apraxia)
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dementia
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loss of cognitive abilities
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alzheimers disease
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most prevalent form of serious age-related dementia, produced by progressive death of neurons in a wide variety of brain regions including neocortex
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gross brain changes in alzheimers brain
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-shrinkage of gyri
-sulci expanded -cortex shrinks -no hippocampus |
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what do PET scans of alzheimers patients show
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severely depressed metabolic activity cuz of no neurons
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why do neurons die in alzheimers disease
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two types of abnormal structures accumulate in areas where neurons are dying: neuritic plaques and neurofibrillary tangles
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what are neuritic plaques
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extracellular accumulations of protein, consisting largely of beta-amyloid protein (A-beta)
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what are neurofibrillary tangles
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abnormal intracellular aggregates of a microtubule-associated protein called tau
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what is tau
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normal component of microtubules that helps stabilize the polymers of tubulin molecules
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what does dephosphorylated tau do
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binds to tubulin and stabilizes microtubules
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what does phosphorylated tau do
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dissociates from tubulin, destabilizing microtubules
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what molecule myperphosphorylates tau in alzheimers disease
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cyclin-dependent kinase 5 (cdk5)
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what occurs as a result of hyperphosphorylated tau
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chronic disruption of microtubules, which may kill neurons
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how is A-beta produced
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selective proteolytic of a protein called amyloid precursor protein (APP) which is a normal component of neuronal membranes
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what is A-beta like normally
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soluble, and doesnt accumulate in the extracellular space of the brain. it is cleared into CSF
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A-beta in alzheimers disease
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insoluble, accumulate into plaques
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what are secretases
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proteases that release A-beta
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what does beta-secretase do
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cuts off most of the extracellular part of APP
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what does gamma-secretase do
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cuts within the membrane to release A-beta
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two forms of A-beta produced, which is more toxic and why
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40 amino acids or 42 amino acids, the latter is toxic because its more hydrophobic
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what has been shown to produce familial alzheimers disease (early onset that progresses rapidly)
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variety of mutations in APP
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where are mutations for alzheimers
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-within A-beta portion of APP or at other sites that inc production of A-beta
-mutations in presenilin, component of gamma-secretase complex responsible for cleavage of A-gamma |
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when is synthetic Alpha-beta toxic
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when applied to cortical and hippocampal neurons in culture or in vivo
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why is A-beta toxic
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-inflammation
-excitotoxicity -synaptotoxicity -decreased spontaneous action potential activity |
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inflammation of A-beta
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local inflammation which may damage surrounding neurons
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excitotoxicity of A-beta
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neuronal death induced exogenous A-beta can be lessened by NMDA receptor blockers. thus, A-beta may cause depolarization which allows Ca in through NMDA receptors
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synaptotoxicity of A-beta
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exogenous A-beta causes reduced numbers of dendritic spines in hippocampal neurons and loss of excitatory synapses
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treatments of alzheimer's disease
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-anti inflammatory drugs
-reducing production of beta and gamma-secretase inhibitors; promoting alpha-secretase -reducing oligomerization of A-beta (prevents formation of dimers) -up-regulate enzymes that degrade extracellular A-beta -neuroprotective compounds; try to prevent neuronal death causes by excitotoxicity or prevent loss of synapses |