Alzheimers

Neuroscience Psb2000 with Orenda Johnson at Florida State University

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By: brittany maloney
Created: 2012-04-15
Size: 19 flashcards
Views: 9

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Dementia: Cognitive symptoms

• Impairment in memory & cognition, accompanied by decreased ability to relate/function athome/work/social settings

Dementia: noncognitive symptoms

Delusions, suspicions, hallucinations, agitation, depression

–Up to 2/3 of AD patients develop delusions & hallucinations

–Depression & dementia are often comorbid…have to distinguish b/t the two

–Also have to distinguish b/t dementia and psychosis

What are the 4 As of Dementia?

• Amnesia–Loss of memory (working memory goes 1st)

• Agnosia–Loss of ability to recognize objects

• Apraxia–Loss of knowledge about how to do things

• Aphasia–Loss of speech

What are some symptoms ofAlzheimer’s Disease (AD)?

• Deficits in explicit & implicitmemory

–Better procedural than declarative memory

–First symptoms can be mild anterograde amnesia

• Gradual progression to more serious memory loss –Language probs (loss of vocab) –Confusion–Depression–Restlessness–Hallucinations–Delusions–Sleeplessness–Loss of appetite

• “Sundowning”

• End stage is usually coma; deathusually caused by an infection

Early onset AD

–People <40 yr old

–Only about 1% (or up to 10%) of people w/ AD

–Gene on chromosome 21 (for APP…don’t want 3 copies of this)

–Gene for ApoE4 which breaks down beta-amyloid (this version isn’t very good at it)

–Mutations in presinilin (part of family of enzymes that chop APP into beta amyloid) can increase risk

–Other genes on other chromosomes linked to more of these cases

Late onset AD

–Over 60 yr old

–5% of people b/t 65-74 yr old

–50% of people over 85 yr old

–Some genes that increase risk, but only account for smallpercentage of cases

–Half of patients have no known relative with A.D.

–Yoruba people (Nigeria): lots of A.D. genes; very little A.D.

•Diet may be protective (low-calorie, low-fat, low-sodium)

What do the neurons and the brain of an AD patient look like?

•Brain atrophy

–Loss of neurons

–Loss of spines & synapses

–Loss of connections between neurons

•Proteins fold abnormally, clump,and interfere w/ neuronal activity

Losing dendrytes, spines and synapses, so eventually entire cell will degrade, neurons like thin sticks, and brains with huge gaps and spaces

Plaques

outside of neurons, includes parts of degenerated neurons

- amyloid precursor protein(APP) makes ab42 which kills neurons, aggregations of A-beta 42 and pieces of dead neuron forms^^^

(formed from degenerating axons& dendrites, in the places b/t neurons)

Tangles

within membrane of a dead neuron

formed from chunks of messed up tau and other parts of a dead neuron

What are some treatment optionsfor Alzheimer’s Disease?

• Drugs to stimulate Acetylcholinereceptors or prolong Ach release

–Ach system is 1st to go –One area damaged (basal forebrain) is important in Ach system& for arousal

• NMDA receptor antagonists toblock excitotoxicity

• Anti-inflammatory drugs(inflammation may be caused by plaques and lead to neuronal dysfunction)

What are some treatment options for Alzheimer’s Disease? cont

•Drugs to stimulate cannabinoid receptors

–Limits overstimulation by glutamate

• Immunization

–to produce antibodies against b-amyloid

–Researched in mice & humans (a few life-threatening side effect in humans though, so research stopped)

• Memory books, respite for caregiver (gives them breaks)

Korsakoff’s Syndrome causes

• Brain damage caused by prolonged thiamine (vitamin B1)deficiency

–Usually in alcoholics: poor diet: lots of carbs; no vitamins

–Thiamine needed to metabolize glucose (fuel for the brain)

•Shrinkage of neurons, esp. in mammillary bodies & dorsomedial nucleus of thalamus, which sendsaxons to prefrontal cortex

•Damage of axons & myelin

Korsakoff’s Syndrome symptoms

•Apathy, similarto damage to PFC; confusion

•Retrograde & anterograde amnesia

•Better implicit than explicitmemory

•Difficulty reasoning thrumemories (ex. what event happened first?)

•Confabulation: person takes aguess to fill in blanks of memory

•Eye abnormalities (nystagmus, oculomotor paralysis, paralysis of conjugate gaze)

•Ataxia of stance and gait

Parkinson’s Disease causes

–Genetics? Yes for early-onset

–Toxins? MPTP à MPP, which is toxic to SN neurons

•Exposure to MPTP or similar chemical in pesticides andherbicides

–Drugs: cigarettes & coffee decrease vulnerability;marijuana increases vulnerability

–Virus? PD symptomsin people w/ and who had encephalitis (swelling of brain)

–Head trauma?

Parkinson’s Disease symptoms

•Rigidity, muscle tremors,slow movement, difficulty initiating movement (or cognitive activity)

- Hunched over shoulders and shuffling steps

•Dementia can be similar to AD,but movement problems are first and predominant sign in PD

–Depression

–Deficits in memory and reason

Parkinson’s Disease treatment

•L-DOPA (can cross BBB bc dopamine won't)

–Doesn’t help in late stages

–Doesn’t prevent continued loss of neurons

–Side effects

Huntington's Disease causes

•Genetic (autosomal dominant)

–95% penetrance

–Chromosome 4

–Trinucleotide repeate (C-A-G)

–Normal gene makes protein huntingtin

–More repeats -> get it earlier

–Earlier it begins -> quicker it progresses

–Abnormal huntingtin harms neurons by:increasing NT release, decrease BDNFrelease, impairs mitochondria

Huntington's disease symptoms

•psychiatric symptoms, which oftendevelop prior to movement disorders

–Depression & anxiety

–sleep disorders

–memory impairment

–Hallucinations & delusions

–Poor judgement

–Alcoholism & drug abuse

–Sexual disorders

•Arm jerks & facialtwitches,later tremors&writhing

For PD, HD and Korsakoff’s, what brain regions areinvolved?

Korsakoff's- mammillary bodies, parts of thalamus, parts of PFC

PD- basil ganglia,substantia nigra

HD- caudate and putamen

About this deck

By: brittany maloney
Created: 2012-04-15
Size: 19 flashcards
Views: 9

About StudyBlue

“Simply amazing. The flash cards are smooth, there are many different types of studying tools, and there is a great search engine. I praise you on the awesomeness.”
Dennis