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67 Cards in this Set

  • Front
  • Back

factors in remembering things

age--better when we are younger




repetition and retrieval--things that are repeated exposed to activate learning mechanisms like LTP and snyaptogenesis




emotion--high levels of emotion (good or bad) can enhance memory




sleep--good, sufficient, restful sleep enhaces memory



brain damage

the damage or death of neurons due to injury or other insult

necrosis

1. accidental cell death


2, DOES NOT REQUIRE SIGNALING AND GENE EXPRESSION


3. cell swelling-which causes bursts


4. cell lyses (swells and bursts), spilling content


5. inflammation


larger damage to cell

apoptosis

1. "cell suicide"--very orderly


2. requires signaling and gene expression


3. cell shrinkage


4. cellfragnments into apoptotic bodies--like


5. clean pieces--no inflammation


6. smaller damage to cell

key points regarding necrosis and apoptosis

1. necrosis represents immediate consequence and apoptosis secondary consequences


2. both represent continuum. some very damaged cells die by necrosis immediately and less damaged may die later in apoptosis


3. apoptosis occurs so that damaged cells not functioning normally don't adversely affect tissue function

causes of brain damage

1. cerebrovascular disorders


2. brain tumors


3. physical trauma


4. infections


5. drugs and neurotoxins


6. neurodegenerative diseases

cerebrovascular disorders

a group of brain dysfunctions related to diorders of the blood vessels supplying the brain

2 types of berebrovascular disorders causing brain injury

aneurysms and cerebral hemorrhage




thrombus and cerebrovascular occlusion

aneurysms and cerebral hemorrhage

weakening of a blood vessel and if it bursts the seepage of blood into brain areas around it, caused by high blood pressure

thrombus and cerebrovascular occulusion

blockage of a cerebral artery, often caused by atherosclerosis, a disease in which excess fats in the diet are deposited into blood vessels and blood clots form

mechanismsby which neurons die in cerebrovascular disorders

1. crushing and compression of neurons by bleeding and hematoma (swelling mass of blood--clotted or unclotted)


2. ischemia

ischemia

lack of blood (and thus O2 and glucose) delivery to "downstream" neurons causes both necrosis and apoptosis, occurs in both cerebral hemorrhage and cerebrovascular occlusion

hematoma

causes death by necrosis, occurs in both cerebral hemorrhage only

how does ischemia cause death of neurons in necrosis

energy defecit--lack of oxygen and glucose disrupts ato production, cells swell and burst whe pumps fail




lactic acidosis--buildup of lactic acid from anaerobic metabolism poisons cells and causes pumps to fail

how does ischemia cause death of neurons in apoptosis

oxidative stress


glutamat excitotoxicity


inflammation

exodative stress

buildup of metabolic intermediates due to abnormal ATP production in the absense of oxygen that damage DNA, proteins, and membranes--causes the small damage if built up

glutamate excitoxicity

hypoxic (lack of oxygen) neurons release excess amounts of the NT gultamate, which causes huge calcium influx into postsynaptic neurons, which triffers apoptosis

inflammation

immune cells from necrosis can also accidently kill neurons by releasing substances that trigger apoptosis

brain tumors

large, excessively proliferating masses of cells in the brain or spinal cord

main times of brain tumors

glioma


secondary mestastases


primitive neuroectodermal tumor (PNET)


meningloma

glioma

glial cell tumor, very aggressive--rapidly growing, mostly found in adults

secondary metastases

tumors that form elsewhere in the body and invade into the brain from the bloodstream, very aggressive, typically found in adults

PNET

very aggressive tumor formed from neural stem cells in young children only

meningioma

tumor of the meninges that grow outside the brain, typically very slow growing, typically found in adults

neural changes and brain tumors in necrosis

compression due to tumor growth--crushes and kills neurons by necrosis, also causes neuronal misfiring

neural changes and brain tumors in necrosis and apoptosis

compression of blood vessels due to tumor growth--occludes blood supply, can cause ischemia and death of neurons by necrosis and apoptosis




tumor hijacking of blood supply of nutrients and oxygen

neural changes and brain tumors in apoptosis

inflammation--immune cells attacking tumor release substances that cause neurons to die by apoptosis

traumatic brain injury (TBI)

damage caused by a blow to the head

sources of injury in TBI

1. coup


2. contrcoup


3. hematoma


4. edema

coup

the inital or primary injury to the brain from the skill striking an object

contrcoup

injury to the opposite part of the brain caused when the brain rebounds and slams into the other side of the skill

hematoma

swelling mass of blood leaking into brain from torn blood vessels and pressing on brain tissue

edema

swelling of brain tissue as a consequence of fluid accumulation in response to trauma

how do neurons die with TBI with necrosis

primary brain injury--due to phsysical damage of neurons due to coup, contrcoup, hematoma and edma

how do neurons die with TBI with necrosis and apoptosis?

compression of blood vessels due to hematoma




decreased blood supply due to tearing of blood vessels

how do neurons die with TBI and apoptosis?

inflammation




glutamate excitotoxity

TBI vs concussion

1. concussion milder form of TBI


2. in concussion, neurons typically injured more than death

infectious encephalitis

infection of the brain by microorganisms

two main types of infectioius organisms causing encephalitis

1. viruses


2. bacteria

4 examples of viral brain infections

1. rabies


2. herpes simplex virus


3. polio


4. west nile virus

rabies

infects through animal bites and moves into cns via infected sensory nerves

herpes simplex virus

infects through breaks in skin and enters cns via infected sensory nerves

polio

infect through GI tract and move and enters cns by infecting nerves of the gut, kills motor neurons

west nile virus

infect through insect bite and enther cns via infected sensory nerves

neural changes in brain infections

1. necrosis of neuronal cels by viral lysis or bacterial toxin


2. immune system tells infected neurons to die by apoptosis

drugs and neurotoxins

destructions of neural tissue by ingested toxis substances

sources of common neurotoxic substances

1. indutrial pollution--heavy metals like mercury, lead, or arsenic


2. synthetic drugs--moto, synthetic THC, K2, spice

neural changes caused by neurotoxins in necrosis

necrosis of neuronal cells by the toxin

neural changes caused by neurotoxins in apoptosis

inflammation--immune system may accidentally kill some neurons while cleaning out necrotic cells




glutamate excitotoxicity--some neurotoxins trigger excitotoxicity

recovery from brain injury

1. increased synaptic transmission


2. increased synaptogenesis


3. increased neurogenesis in key brain regions like the hippocampus


4. rehabilitation often involves activities which increase or strengthen these


5. recovery from brain injury is a form of learning

neurodegenerative diseases

diseases that result in the progressive destruction of neurons

key points regarding neurodegenerative diseases

1. not until late adulthood


2. progessive--get worse over time


3. no cure for them, only treat sympotoms


4. neurons typically die by apoptosis unlike other forms of brain damage

3 ex of neurodegenerative diseases

1. huntington's disease


2. alzheimer's disease


3. parkinson's disease

huntington's disease

1. degeneration and death of neurons predominantly in the basal ganglia and cortex


2. inherited or genetic disorder

symptoms of huntingtons's disease

chorea, jerky movement


dementia (decision making)


anxiety, depression, blunted affect, egocentrism, and compulsive behavior

brain changes in huntingtons disease

generalized and progressive brain atrophy, particularly in the cerebral cortex and basal ganglia

basal ganglia

important in producing voluntary movement and inhibiting involuntary movement

neuropathological changes in huntington's disease

huntington protein misfolds and creates inclusion bodies

inclusion bodies

disrupt gene expression, calcium signaling, and mitochondrial function, and may also lead to apoptotic cell death bc normal huntington inhibit apoptosis

alzheimer's disease

degeneration and death of neyrons preminantly in the limbic system and cerebral cortex

cause of alzheimer's disease

unknown, but genetics, infection, head injury/TBI, high blood pressure and heart disease

symptoms of alzheimer's disease

cognitive--dementia, defects in attention, impaired explicit memory, language difficulties (aphasia)




emotional--depression, irritability, aggresion




implicit memory




motor--apraxia, difficulty putting together coordinating movements, danger of falling

brain changes in alzheimer's disease

death of cholinergic neurons in the basal forebrain, important for attention




death of neurons in the medial temporal corttex and hippocampus, memory consolidation and storage




death of neurons in the prefrontal and other parts of the cortex and limbic system, working memory and emotion regulation

neuropathological changes in alzheimer's disease

abnormal folding of amyloid protein with other protein called tau in neurofibrillary

parkinson's disease

degeneration and death of dopaminergic neurons within the substantia nigra

parkinson's disease cause

genetics, infections, pesticide/herbicide, exposure, trauma

sympotoms of parkinson's disease

motor--tremor of head and exptremities, rigid and difficulty producing voluntary movements, slow movements (bradykinesia)




cognitive--dementia or progressively impaired cognitive function (especially decision making)




mental--depression