PSYCH 265 1st Edition Lecture 29Outline of Last Lecture I. Brain areas affects in schizo & parkinson’s II. EPSIII. Extrapyramidal motor controlIV. Signs of EPSV. Etiology of TDVI. Treatments of drug abuse VII. Abuse potential of neuroleptics VIII. Genetics of schizophrenia Outline of Current Lecture I. ADHD a. Types b. Monoamine hypothesis c. Neurochemistry d. Anti-adhd stimulants e. Atomoxetine f. Abuse of neurostimulantsII. Dementia a. Common causeThese notes represent a detailed interpretation of the professor’s lecture. GradeBuddy is best used as a supplement to your own notes, not as a substitute.b. Causes c. SymptomsIII. Alzheimer’s a. Pathology IV. Neurofibrillary tangles V. Senile plaquesVI. ChE-ICurrent Lecture-ADHDoOne of most common childhood disorders & can continue through adolescence & into adulthoodoAffects 9% American children aged 13-18 yoBoys 4x at risk than girls oAffects 4.1 American adults aged 18 and older oStudies show that the number of children being diagnosed with ADHD is increasing but unclear why-Types of ADHDoInattentive type Ease of distraction w/ focusing & organizing oHyperactive-impulseFidgety, restless, trouble staying quite, impatient oCombined -Monoamine Hypothesis of ADHD oHave variations of the transporter genes for these neurotransmitters oPatients with predominantly inattentive ADHD have changes in NE transporter geneWhich affects NE levels in brain oPatsies with predominantly hyperactivity-impulsive ADHD have changes in DA transport gene, thus affecting DA levels in brain oPatients with conduct disorder & mood problems that accompany ADHD have changes in serotonin transporter geneAffecting serotonin levels in brain -Neurochemistry of ADHD oSings & symptoms of ADHD are attributed to a deficiency of NE and/or DA-Anti-ADHD neurostimulants oBlock the reuptake of & cause neuronal release of NE & DA-Atomoxetine (straterra)oAtomoxetine is a non-stimulant that blocks NE reuptake-Abuse of neurostimulants oWhen misused, neurostimulants can cause addiction oCommon misperception that use of neurostimulants for treatment of ADHD leads to drug addiction oMost adolescents & adults who abuse stimulants do not have ADHD Some of these people learned how to present as though they have ADHD in order to obtain stimulants-Abuse of neurostimulants oGrowing number of teens & young adults are abusing prescription stimulants to boost their study performance in an effort to improve their grades in school and there is a widespread belief that these drugs can improve a persons ability to learn (cognitive enhancement)oPrescription stimulants do promote wakefulness but studies have found that they don't enhance learning or thinking ability when taken bay people who do not actually have ADHD Research has shown that student who abuse prescription stimulants actually have lower GPAs in high school and college than those who don’t-Do prescription stimulants affect a patients risk of substance abuse?oStudies show have found no differences in later substance use for children with ADHD who received treatment & those that did notoSuggests treatment w/ adhd medication appears not to affect (either negatively or positively) an individuals risk for developing a substance use disorder- Dementia oLoss of mental functions such as thinking, memory, and reasoning that is severe enough to interfere with a persons daily functioning oNot a disease itself but a group of symptoms that are caused by various diseases or conditions oSymptoms can also include changes in personality, mood, and behavior oTrue dementia cannot be cured-Most common cause of dementiaoDevelops when parts of the brain that are involved w/ learning, memory, decision making, and language are affected by one or more of a variety of diseases or infections oMost common cause is alzheimer's diesease but there are as many as 50 other known oAlzheimer's causes 50-60% of all dementias -Causes of dementia oAlzheimer's oVascular dementia oDementia w/ lewy bodies (DLB)oMixed dementia oParkinson's oFrontotemporal dementia oCreutzfeldt-jakob disease oNormal pressure hydrocephalus oHuntington's disease oWericke-koraskoff syndrome -Symptoms of dementia oDifficulty with many areas of mental function:LanguageMemory Perception Emotional behavior or personality Cognitive skills (such as calculation, abstract thinking, or judgment)Usually appears first as forgetfulness-Epidemiology of alzheimer's disease oPrevalence1.6% both overall in 65-74 age group w/ rate increasing to 19% in 75-84 group to42% in greater than 84 groupoIncidence5-8/1000 compared to 10-15/10000 for all dementias Every 5 yrs after age 65 risk of acquiring the disease approximately doubles, increasing from 3-69/1000-Pathology of alzheimer's disease oPost-mortem examination of brains tissues of patients w/ alzheimers disease will reveal the following changes:Neurofibrillary tangles Amyloid plaques-Neurofibrillary tangles oInsoluble twisted fibers found in neurons oConsist of protein called tauForms part of microtubules, which transport nutrients and other substaces from one part of the nerve to anotheroAlzheimer's disease, the tau protein is abnormal and the microtubule structures collapse-Senile plaques oBeta amyloid is a protein fragment snipped from an amyloid precursor protein (APP)oIn healthy brain, these protein fragments are broken down and elminatedIn alzheimers, fragments accumulate to form hard, insoluble plaques-Alzheimer's diseaseoAch neurons in hippocampus play important role in memory oLoss of Ach neurons in hippocampus reduces activation of Ach receptors Resulting in memory loss-Cholinesterase Inhibitors (ChE-I)oPrevent Ach degradation, leading to increased levels of synaptic AchoIncreased activation of Ach receptors slows the loss of memory oImprovement is only temporary as cell death of Ach neurons