[Lecture] Maintaining mental agility
Mar. 16th, 2006 05:24 pm![[personal profile]](https://www.dreamwidth.org/img/silk/identity/user.png){kind=small}
magidSecond Longwood lecture. (Spelling not wholly guaranteed.)
The first speaker was Dr. Aaron Nelson, who spoke about what normal memory is, and how to maintain a good memory. He started with the different kinds of memory, short-term memory, long-term memory (including a lot of categories, such as procedural, episodic, semantic, and so on), and a sort-of other category, memory for faces. We get sensory information, and by paying attention to it, it makes it into short-term memory. Rehearsing (re-using, re-thinking) that then moves it into long-term memory.
Where is memory? In widely distributed networks in the brain, though individual memories can be located in one place, as shown by which neural networks fire.
As we age, we lose brain matter and white matter (I don't remember how this was different, though). Neurotransmitters decrease over time as well. Forgetting things like names, why you came to a room, where you parked, and so on is normal, and not an indication of dementia.
How can we keep our brains functioning well?
And, of course, it's important to use the brain, both for intellectual pursuits (challenging ones especially) and for social ones (socially connected people tend to have better cognitive function).
The second speaker was Dr. Dennis Selkoe, and he focused on Alzheimer's disease (and a bit about other kinds of dementias). When I heard the topic, I wasn't as interested, but he made it fascinating.
He started with an animation of a neuron firing, then going the synapse cold. The most common form of dementia, Alzheimer's, is caused by synaptic failure.
Who's likely to get dementia? Everyone's likely, there aren't different rates based on gender or race (though later there's a emendation to this). There is no cure (now, anyway), and it is fatal, decreasing life expectancy by a third or more. (There was a side discussion here of why 65 is the cutoff for things like retirement and age-related diseases, and it turns out it's Bismarck's fault: they were trying to determine at what age to offer pensions, and asked Bismarck when the average German died. Around 65 was his answer, so that was when pensions kicked in, obviously minimizing costs for the state.)
There are a variety of different kinds of dementia, including Alzheimer's, vascular, Parkinson's, dementia with Lewy bodies, frontotemporal dementias, and "prion" dementia (such as mad cow and Kreutzfeld-Jacob).
We saw pictures taken from brains of people who'd died with late-stage Alzheimer's. There were plaques of amyloid-β and neurofibrylary tangles, which are characteristic of Alzheimer's late stage, but not in healthy brains. This lead to the current hypothesis that an imbalance between production and removal of amyloid-β protein is the cause of Alzheimer's. ["This is your brain. This is your brain on amyloid-β."]
People with Down's syndrome have an extra copy of the amyloid parent protein, which is carried on the incorrectly doubled gene. There are other genetic defects that can lead to greater amyloid-β production, especially amyloid-β42, which leads to a higher risk of Alzheimer's.
He described an experiment where doublets and triplets of amyloid-β was injected into mice who'd already learned a sequence of numbers of times to push a lever (the positive integers given by the function x2 - x, actually). After the injection, they started making a couple of different kinds of errors. So far, it seems that multiples (doublets and triplets, etc) of the protein are much worse for people than the single copies. And this also gives hope that there will be therapies for Alzheimer's, such as a inhibiting amyloid-β-generating enzymes, a vaccine to prevent doublets, or something to prevent inflammation around injuries to neurons.
The question and answer session worked much better than last time, with the moderator, Dr. Deborah Blacker, joining the other two at a table where they could review the questions together and make sure the right person had them to answer. As one talked, the others could classify or group questions, and they were able to answer a lot more of them much more efficiently.
P.S. If you'd like to view the lecture directly, it will be online here (there are already links to the last one on genetic testing.
The first speaker was Dr. Aaron Nelson, who spoke about what normal memory is, and how to maintain a good memory. He started with the different kinds of memory, short-term memory, long-term memory (including a lot of categories, such as procedural, episodic, semantic, and so on), and a sort-of other category, memory for faces. We get sensory information, and by paying attention to it, it makes it into short-term memory. Rehearsing (re-using, re-thinking) that then moves it into long-term memory.
Where is memory? In widely distributed networks in the brain, though individual memories can be located in one place, as shown by which neural networks fire.
As we age, we lose brain matter and white matter (I don't remember how this was different, though). Neurotransmitters decrease over time as well. Forgetting things like names, why you came to a room, where you parked, and so on is normal, and not an indication of dementia.
How can we keep our brains functioning well?
- Cardiovascular fitness: brain health parallels heart health. Exercise also helps with brain plasticity. (And one of the articles in the handout suggests that getting a variety of different kinds of exercise is even better.)
- Nutrition: eating well to get sufficient vitamins and minerals. There was a quick discussion of taking supplements, and he suggested reading a book by Walter Willet, which I think is this one (he has others).
- Alcohol: a moderate amount (one or two drinks per day) may be protective, but don't start drinking just for this.
- Sleep: it's necessary for memory consolidation, as well as restorative and helping alertness (if it's good-quality sleep, of course).
- Stress: mild stress can enhance focus, while severe stress is more of a problem, and can lead in time to damage in the hippocampus. Insert bad pun here.
And, of course, it's important to use the brain, both for intellectual pursuits (challenging ones especially) and for social ones (socially connected people tend to have better cognitive function).
The second speaker was Dr. Dennis Selkoe, and he focused on Alzheimer's disease (and a bit about other kinds of dementias). When I heard the topic, I wasn't as interested, but he made it fascinating.
He started with an animation of a neuron firing, then going the synapse cold. The most common form of dementia, Alzheimer's, is caused by synaptic failure.
Who's likely to get dementia? Everyone's likely, there aren't different rates based on gender or race (though later there's a emendation to this). There is no cure (now, anyway), and it is fatal, decreasing life expectancy by a third or more. (There was a side discussion here of why 65 is the cutoff for things like retirement and age-related diseases, and it turns out it's Bismarck's fault: they were trying to determine at what age to offer pensions, and asked Bismarck when the average German died. Around 65 was his answer, so that was when pensions kicked in, obviously minimizing costs for the state.)
There are a variety of different kinds of dementia, including Alzheimer's, vascular, Parkinson's, dementia with Lewy bodies, frontotemporal dementias, and "prion" dementia (such as mad cow and Kreutzfeld-Jacob).
We saw pictures taken from brains of people who'd died with late-stage Alzheimer's. There were plaques of amyloid-β and neurofibrylary tangles, which are characteristic of Alzheimer's late stage, but not in healthy brains. This lead to the current hypothesis that an imbalance between production and removal of amyloid-β protein is the cause of Alzheimer's. ["This is your brain. This is your brain on amyloid-β."]
People with Down's syndrome have an extra copy of the amyloid parent protein, which is carried on the incorrectly doubled gene. There are other genetic defects that can lead to greater amyloid-β production, especially amyloid-β42, which leads to a higher risk of Alzheimer's.
He described an experiment where doublets and triplets of amyloid-β was injected into mice who'd already learned a sequence of numbers of times to push a lever (the positive integers given by the function x2 - x, actually). After the injection, they started making a couple of different kinds of errors. So far, it seems that multiples (doublets and triplets, etc) of the protein are much worse for people than the single copies. And this also gives hope that there will be therapies for Alzheimer's, such as a inhibiting amyloid-β-generating enzymes, a vaccine to prevent doublets, or something to prevent inflammation around injuries to neurons.
The question and answer session worked much better than last time, with the moderator, Dr. Deborah Blacker, joining the other two at a table where they could review the questions together and make sure the right person had them to answer. As one talked, the others could classify or group questions, and they were able to answer a lot more of them much more efficiently.
P.S. If you'd like to view the lecture directly, it will be online here (there are already links to the last one on genetic testing.