PSYC 372 Lecture Notes - Lecture 11: Amyloid Beta, Anterograde Amnesia, Retrograde Amnesia
26 Apr 2018
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Lecture 11 Notes
• Alzheier’s Disease
i. A major cause of amnesia
a. About 5% of people ages 65-74, and almost 50% of people over 85
ii. Mild memory impairment progresses to dementia
a. Simple everyday activities become difficult
• Meor ipairets i Alzheier’s disease
i. Anterograde and retrograde amnesia for declarative (explicit) memories
a. Reeerig fail eers’ aes, gettig aroud to, et.
ii. Deficits in non-declarative memory for verbal and perceptual material
a. Incomplete figures test
iii. No impairment in sensorimotor learning
a. Driving a car
• Etiolog of Alzheier’s disease
i. Abnormal clumping of two brain proteins
1. Amyloid plaques: amyloid beta protein (B-amyloid) is cleaved improperly
a. Forms clumps that surround and damage the membranes of axons, dendrites
b. Plaques appear before behavioral symptoms do
c. Mutation in the gene producing B-amyloid linked to early-oset Alzheier’s
disease
2. Tae tagles: disruptio of euros’ iteral support struture
a. Degeneration of neuronal cell bodies
• Brai areas affeted Alzheier’s disease
i. Postmortem studies reveal that plaques and tangles are often abundant in brain areas
important for learning and memory
a. Medial temporal lobe areas
b. Prefrontal cortex
ii. The basal forebrain is also particularly vulnerable
a. Brai’s ajor soure of aetlholine (ACh)
b. Large reduction in ACh leads to disruptions in cognition and memory
• Treatets for Alzheier’s disease
i. No treatment can currently cure or stop progression
ii. Acetylcholinesterase (AChE) inhibitors (Aricept) and memantine (glutamate receptor
antagonist) are moderately effective in some patients
iii. Healthy diet may prevent progression
a. Curcumin (component of turmeric; an Indian spice) reduces plaques in aged mice
❖ Antioxidant and anti-inflammatory properties
iv. Vaccine against B-amyloid is currently being tested
• Korsakoff’s “droe
i. Brain damage caused by prolonged deficiency of thiamine (a B vitamin)
ii. Shrinkage of neurons throughout the brain, especially in the diencephalon
a. Medial thalamus and hypothalamus
• Meor ipairets i Korsakoff’s sdroe
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i. Starts with anterograde amnesia for declarative memories
a. Confabulation: filling in the gaps of a memory/story with made-up information
❖ Often more pleasant than what actually happened
ii. Progresses to retrograde amnesia that can extend back to childhood
iii. Less severe impairments in non-declarative memory
• He’s theor o the eural ehaiss of learig 949
i. Axon of neuron A repeatedly stimulates receptors on dendrites of neuron B
a. In the future, A is more likely to excite B because the connection between A and B
has strengthened
b. Cells that fire together ire together
ii. Testig He’s theor
a. 1973: Bliss and Lomo applied high-frequency electrical stimulation to neurons in the
hippocampus
b. Produced long-term increases in synaptic transmission involving the stimulated
neurons
• Long-Term Potentiation (LTP)
i. The stimulation produced exactly what Hebb proposed to be occurring during learning
ii. Stable and enduring strengthening of synapses following repeated stimulation
a. Real-life stiulatio = learig e iforatio
• LTP and Glutamate
i. LTP shown to depend on changes at synapses that release glutamate
ii. 2 types of glutamate receptors
1. AMPA
2. NMDA
• Glutamate synapses and learning
i. Animal studies show that functional and structural changes occur at glutamatergic
synapses after learning
a. Presynaptic neurons release more glutamate
b. Postsynaptic neurons have more glutamate receptors
c. Increased number and size of dendritic spines on postsynaptic neurons
• Effects of manipulating LTP on learning
i. Doogie ie: trasgei ie ith higher uers of NMDA-type glutamate
receptors
a. Superior learners
ii. AMPAR knockout mice: lack AMPA-type glutamate receptors
a. Deficits on multiple memory tasks
• Memory can be classified into several different types, each of which are thought to be sub
served by specific brain areas
• The case of patient H.M. led to the study of the neural bases of learning and memory in both
humans and nonhuman animals
• Alzheier’s ad Korsakoff’s diseases are fors of seere eor loss that ste fro speifi
neurobiological abnormalities
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
A major cause of amnesia: about 5% of people ages 65-74, and almost 50% of people over 85. Mild memory impairment progresses to dementia: simple everyday activities become difficult, me(cid:373)or(cid:455) i(cid:373)pair(cid:373)e(cid:374)ts i(cid:374) alzhei(cid:373)er"s disease. Anterograde and retrograde amnesia for declarative (explicit) memories: re(cid:373)e(cid:373)(cid:271)eri(cid:374)g fa(cid:373)il(cid:455) (cid:373)e(cid:373)(cid:271)ers" (cid:374)a(cid:373)es, getti(cid:374)g arou(cid:374)d to(cid:449)(cid:374), et(cid:272). Deficits in non-declarative memory for verbal and perceptual material. No impairment in sensorimotor learning: driving a car. Incomplete figures test: etiolog(cid:455) of alzhei(cid:373)er"s disease. Postmortem studies reveal that plaques and tangles are often abundant in brain areas important for learning and memory: medial temporal lobe areas, prefrontal cortex. The basal forebrain is also particularly vulnerable: brai(cid:374)"s (cid:373)ajor sour(cid:272)e of a(cid:272)et(cid:455)l(cid:272)holine (ach, large reduction in ach leads to disruptions in cognition and memory, treat(cid:373)e(cid:374)ts for alzhei(cid:373)er"s disease. No treatment can currently cure or stop progression. Acetylcholinesterase (ache) inhibitors (aricept) and memantine (glutamate receptor antagonist) are moderately effective in some patients.
