Lecture 17 Flashcards
What do we need to know about Constructing rich false memories of committing crime, Medial Temporal lobe causes deficits in episodic memory and episodic future thinking not attributable to deficits in narrative construction.
these are three readings she assigned. She embedded all of them into her lectures. She pulled out some of the highlights. If you read them and attend class you’ll be okay. She will not test you on obscure details.
Francis and Maria led a discussion on these papers. Not all of it was picked up by the recording. They presented these articles and had a class discussion about the key methodological differences between these papers. She is interested to know what are the differences that may have produced different results. Remember the theoretical framework of these papers is about context dependent learning.
Video on
“The BHAMM Study: Exploring Sex, Gender, and Diversity in Midlife Brain Health” by N. Rajah
she’s not going to tests us on the nitty gritty of stats etc but she wants to hear about what we learn from learning about brain health and memory.
Why do we care about lifespan learning?
● Allows us to explore individual differences in development and ageing/aging
● Teaches us about plasticity
● Allows us to maximize our potential
this lecture is interesting from the point of view of memry science but also the practicalities of daily life and strokes etc.
What is memory development like in infancy and childhood?
Caveats before we begin:
● Developmental trends represent averages across considerable variability.
● Variability exists within a cohort (e.g., the huge diversity of standardized test scores for high school seniors; diversity in language acquisition).
● Variability also exists across developmental trajectories.
variability is something we have to keep in mind, particularly relevant to people with children and children’s abilities to learning how to read. When we’re looking at a mean we need to know what the variability is. What is the min and max?
Immediately after birth, human infants demonstrate incredible learning abilities:
- language
- social skills
- motor abilities
● Some limitations are evident due to immature sensory and motor systems.
● Note that there is even evidence of learning in fetuses.
we don’t necessarily see the output of language skills until a bit later.
Non-declarative memory in infants?
Non-declarative Memory in Infants?
● 2-month-old infants learned to kick to move a colourful mobile (instrumental conditioning)
● If crib liner with a new pattern was used, babies didn’t kick (context- dependent learning)
● Human and rat infants learn eye-blink conditioning (classical conditioning)
2 month old infants learn to kick to move a colourful mobile. If you change the lining in their crib, they don’t kick. That is context dependent learning. They are learning that in this specific context, if I engage in this behaviour this is the outcome, but when you change some of those cues they don’t engage in the behaviour.
Development of declarative memory?
Development of Declarative Memory?
● Declarative memory is difficult to study in young children because they do not have the verbal skills to “declare” what they remember
● Declarative memory studies are conducted in children who are old enough to speak
a big question many people ask is the development of declarative memory. This is difficult to study in babies because they are pre-verbal There is an idea that episodic memory doesn’t develop until later in life and this is why amnesia is not necessarily detected until school age. It is difficult to study these forms of memory becuase they need to declare their knowledge.
Study of development of declarative memory?
Development of Declarative Memory
Study:
● Children were provided with sentences:
○ “What animal can’t make any sounds?”
○ Presented by an experimenter or a puppet
● Test (1 week delay):
○ “What animal can’t make any sounds?” (semantic memory)
○ Semantic recall increased with age
○ Who said it =episodic memoryà how do children do?
● See next slide
they did this with puppets vs. experimenters. After 1 week the children came back in the lab and tested their memory. In this case the answer is giraffe. So they assessed whether these children from 4-8 could remember these facts. They found that semantic abilities increased with age. They were most interested in the episodic memory piece with a source memory test. They asked who did you hear this info from? Was it the experimenter, the puppet, or someone else. Sometimes you have a memory of the expeirence but you mixed up the source.
Episodic Memory in Children: Who said it?
Correct source: episodic memory (improves with age)
Intra-experimental (incorrect source, mixed up puppet with experimenter) Extra-experimental (incorrect source, thought learning of fact took place outside of lab)
if episodic memory is good we want to see high correct source. When 4 year olds make a mistake, they are making extra experimental so errors. 6 and 8 year olds show an increase in correct source. What goes down is the extra experimental errors.
they asked them who said this. They could give a correct response (they get the source correct), they could make an intraexperimental error (incorrect source, they are mixing up the puppet etc. . They could have an extra experimental (maybe they think mom or dad told them).
What are sensitive periods for learning?
● Some learning abilities are only available or more readily available early in life, during the so-called sensitive period or critical period, after which some forms of learning may become difficult or impossible.
(this is an example of a sensitive period.)
● Imprinting: forming a close bond with the first individual seen after birth
○ Common in birds, but also occurs in other species (some mammals)
○ Bond forms best immediately after birth; after this critical period, harder to form
some forms of non-declarative memory appear earlier but declarative memory is harder to assess.
there are sensitive periods for learing. This is the idea that some learning abilities are only/more readily available during sensitive periods. Sensitive periods is better because it implies it is not impossible to learn during this time.
sensitive periods for social attachment?
● In a study, rhesus monkeys were isolated from their mothers (Harlow studies)
● In adolescence, they were moved to group cages
● Showed social deficits
● In many of these studies involving both humans and non-human animals, younger children perform better when exposed to enriched or healthier environments, which can alleviate certain impairments. This exposure should occur earlier in life to be most effective.
many studies were done on monkeys for the amelioration of impairments that developed as a result of social isolation. After a period of time, the question is, can you ameliorate some of the impairments that arise? These studies tend to show that reversal of some of these effects can occur when you restore the environment. This is relevant to humans because people ask if a child has been exposed to a harmful environment early in life, can you reverse or reduce some of the impairments that may have arised from that experience.
Sensitive periods for language?
Sensitive Periods for Language
Some evidence suggests that language must be learned before approximately 12 years of age to reach true fluency.
Skills for phonetic discrimination can diminish during development for sound distinctions not utilized in the languages to which a person is exposed. Individuals become perceptual learning experts for their language.
Although this is a subject of debate, second-language acquisition is generally believed to be easier during childhood.
being able to discriminate speech sounds is easier earlier in life. We kind of become little experts on the perceptual nuances of language.
This is an evolving literature.
Adolescence: Childhood to Adulthood
● Strong development of working memory and central executive function during adolescence through adulthood
teenagers may be more wild in their behaviours because their frontal lobes aren’t developed, there is some truth to that.
Aging Memory: Adulthood to Old Age
Aging Memory: Adulthood to Old Age
● Adult abilities can remain stable for many years
● Unfortunately, the overall trend is a decline in most basic memory and learning skills
● Working memory is often one of the first areas to display age-related decline
● There may be effects related to menopause
we see rapid development in many forms of learning or cognition more broadly. We see a lot of stability in adult years and then we see a decline across the board, Working memory is more or less the first thing to decline.
Aging Memory: Adulthood to Old Age
Similar trends are observed in non-declarative memory: Classical conditioning begins to decline at ages 40 to 50, taking potentially twice as long in older adults compared to young adults. Skill learning decreases rapidly after age 60.
● Semantic and episodic memory exhibit an uneven decline.
● The ability to retain and retrieve older episodic and semantic memories shows
less decline during healthy aging.
○ For instance, seniors who studied Spanish in high school still recall many of the Spanish words learned, even after long periods with little practice.
● Unfortunately, the ability to form new episodic and semantic memories does decline with age.
○ These difficulties can be alleviated with slower rates of presentation and/or meaningful stimuli.
we also see declines in semantic and episodic memory. we tend to see a decline in the ability to learn new facts and episodes.
Some good news: strong compensation
● Although basic skills decline, older adults have more skills and experience to draw on.
● This richer pool of experience can often help compensate for diminished skills and enable performance of complex skills at the same or better level than in young adults!
the richer pool of experience can often help compensate for diminished skills. one point of discussion that comes up in the field of aging is whether some of the impairments we see in older adults is due to stereotype threat. If we say this is to understand age related decline, this might negatively impact your performance.
although we see declines in episodic memory, they actually tend to tell really good stories and provide a lot of semantic content. On an episodic memory task they score lower but their stories are more interesting and more tailored to the audience.
What do we know about the developing brain?
● Human brain development is strongly influenced by both genes and the environment
● Human brain development features competition between cells and synapses; survival seems based on usefulness:
○ Overproduction
○ Competition for a limiting resource
theres a competition for space and resources. Generally speaking, there is likely an overproduction early in life.
The Developing Brain: Competing Neurons
● Neurons are produced very rapidly after conception, at a rate of up to 250,000 per minute.
● Production is mostly complete by 25 weeks, although the connections between neurons are not fully established.
● More neurons are produced than necessary.
● Unsuccessful neurons undergo apoptosis, or programmed cell death, which
may eliminate up to one-third of the neurons initially produced.
● A similar trajectory occurs for synapses, where more are created than needed, and weaker connections are pruned accordingly.
more neurons are produced than we actually need. Then what happens is pruning takes place. This is called apoptosis. This can eliminate up to 1/3 of neurons that are produced. Adolescence corresponds to changes throughout the brain as well. These change can include synaptic changed
Brain Changes in Adolescence
Adolescence corresponds to changes throughout the brain, but especially in the frontal cortex.
Synaptic changes: Strong synaptogenesis (new synaptic connections), especially in the frontal cortex through adolescence, pruning throughout early adulthood
Myelination:
* Recall that axons are wrapped in myelin, improvings peed and fidelity of communication between brain areas; starts after birth, not complete until around 18 years, especially in the frontal cortex
Modulation: * Dramatic increase in dopamine inputs during adolescence
increase in myelination. The axons in the brain are covered in a sheeth. There is also an increase in neurotransmission.
The Brain from Adulthood to Old Age
● Unfortunately, even healthy aging is associated with brain deterioration, including decreased synaptic density
● The loss is uneven across brain areas and correlates with a decline in skills. The frontal cortex shows substantial loss
● Even where the number of neurons and synapses remains stable, the wiring may become less stable and functional
the healthy brain shows deterioriation with aging. For example, as you age, there is less synaptic density. The loss is uneven across the brain. You see notable decline in frontal cortex.
Barnes and colleagues investigated synaptic stability across different ages in rats.
Procedure:
“Place cells” in the rat hippocampus were mapped during exploration of a maze. Rats were returned to the same maze later, and place cells were remapped.
Results:
For young rats, the same place cells encoded identical locations within the maze (top panel). For older rats, the same place cells were activated in different areas of the maze (bottom panel).
Older rats maintained some level of behavioural performance in the maze but exhibited reduced stability in the place cell firing patterns.
These researchers were studying the stability of synapses in rodents. What they did is they were particularly interested in place cells. These are cells that fire in a particular location. In the youn rodents, the place cell firing patterns are really similar in the 2 sessions. They are firing one part of the maze and then are also firing the same part in the second session. Look what happens in the aged rodents? The place cells are still firing but when you look at the second session there isn’t a lot of good correspondance. There is a reduced stability of the place cell firing between the 2 sessions. This exemplifies that even if the number of neurons is there. The way those neurons are operating might differ. Exercise may slow the progression of age related decline and cognition.
● Exercise may slow the progression of age-related decline in cognition
● More research is needed!
What do we know about alzheimer’s disease?
● Alzheimer’s Disease (AD)—a form of progressive cognitive decline from accumulating brain deterioration
● AD accounts for 60-80% of all dementia cases
● AD was the 9th leading cause of death in all Canadians in 2022 according to Statistics Canada
there are different forms of age related decline that veer into the unhealthy category. There is slow decline overtime. Alzheimer’s is one form of dementia but there are other forms of dimentia as well. If they are not showing episodic memory impairments you shouldn’t rule out dimenti because they might have another type of dimentia.
What do we know about Progressive Memory Loss and Cognitive Deterioration
this is different from other forms of dimentia.
in the late stages the forms of dimentia look more similar.
Episodic Memory Loss
(recent visitors) leads to
Semantic Memory Loss
(familiar names, locations) leads to
Conditioning and Skill Learning
In late-stage AD, there is often a lack of awareness and daily living skills
there is degenration of the hippocampal area. then as the disease spreads out ot more laterla parts of the cortex. It spreads out to semantic memory. Then it continues to spread through the whole brain. You see decline of conditioning and skill learning. There is a progression.
Plaques and Tangles—Hallmarks of Alzheimer’s Disease
Plaques and Tangles—Hallmarks of Alzheimer’s Disease
Amyloid plaques = deposits of beta-amyloid (abnormal byproduct of amyloid precursor protein, kills adjacent neurons).
Plaques evenly distributed across cortex.
Neurofibrillary tangles = collapsed protein scaffolding within neurons.
Early in AD, accumulate in hippocampus & MTL.
Hippocampal shrinkage = early AD warning sign.
there are hallmark features in the brain of alzheimer’s disease but we don’t know whats causal and whats correlate. Amyloid plaques are deposits of beta amyloid. It kills neurons and spreads throughotu the cortex. People don’t understand if this is the cause or a correlate. Another marker is tangles which is a collapsing of protein scaffold. Just understand this at the broader level. If the foundation of a house collapses everything else will collapse.
Genetic Basis of Alzheimer’s Disease?
● Several genes implicated in AD.
● Mainly related to early-onset AD (35–50 years).
● Less than 1 percent of AD cases = early-onset
● Environmental influences are important
what is the degeneration in the brain leading to these deficits? We often think of alzheimers as developing later in life but it can develop earlier as well.
Aging Related Brain Damage: Other Examples
● Stroke
○ Leading cause of disability worldwide
○ Affects the arteries that communicate with the brain
○ Part of the brain cannot get the blood (and oxygen)
○ Neurons will die
stroke is the leading cause of disability world wide and it effects the arteries that communicate with the brain. These can stop functioning and this can lead to oxygen deprivation to the brian and when neurons don’t have oxygen they die.
What are the types of strokes?
Types of Stroke
● Ischemic Stroke: a blood clot in an artery obstructs blood flow. Neurons loose their oxygen and glucose supply (more common).
● Hemorrhagic Stroke: blood vessel ruptures. Neurons receive excess oxygen and other substances, which can lead to neuron death (less common).
here the blood can’t flow and isn’t being delivered ot the neurons. Tihis is the more common one.
neurons here receive excessive oxygen.
when people are examining the damage to the brain, people often talk about the core region and the penumbra.
when the neurons arounf have a partial loss this is the penumbra effect
What are the behavioural consequences of stroke?
● Numbness, weakness in the face, arm, leg (one side of body)
● Sudden, severe headache
● Blurred vision
● Confusion, difficulty speaking
● Dizziness, loss of balance/coordination
● Loss of cognitive function, including learning and memory
symptoms tend to present unilaterally.
What is the FAST Acronym?
“If you do nothing else, act quickly to call 911.”
Not an exhaustive list.
Do research on this topic!
FACE: ask them to smile, does one side look like its drooping?
ARM: instruct them to raise both arms, does one drift downward?
SPEECH: ask them to talk does it sound strange?
TIIME: if you observe any of these things call 911 immediately.
What is recovery after brain injury like?
Recovery after Brain Injury
● Recovery after brain injury ranges from subtle to significant
● Recovery can happen at all ages. Though the younger brain may be more
plastic, older brains can show recovery too!
What are the General Mechanisms for recovery?
General Mechanisms
● Restoration of function of neurons that were damaged
○ Change in structure and function of undamaged neurons (e.g., new
synapses)
sometimes the neurons are only partially damaged and they can recover.
● Unmasking: Normally latent (silent) projections become functional following injury to other projections
(lets say primary motor cortex is affected by a stroke, other parts of the brain that support motor functioning can take over. )
○ Can help with the formation of new behavioral strategies to perform affected functions
What are the principles of recovery?
Principles of Recovery
● Recovery is better in infants and children
● -Developing nervous system shows more rearrangement, compensation
and growth
- e.g., stroke in infants = substantial functional recovery
How do you promote recovery?
Promoting Recovery
● 1. Behavioral rehab
e.g., practice, exercise, motivation
● 2. Drugs (mostly to prevent further damage; subsequent strokes)
● 3. Experimental approaches (e.g., transcranial magnetic stimulation to
promote plasticity)
● Video
WATCH VIDEO
there is behavioural rehab, theres drugs avialable designed ot prevent future stroke, experimental approaches.
