My previous three
posts constitute quite an astonishing thing: a kind of neurological
case for something like a human soul. Each of the posts presented an
argument for the claim that your brain cannot be storing all your
memories. One argument was based on the apparent impossibility of
the brain ever naturally developing all of the many encoding
protocols it would need to store the many different things humans
store as memories. The second argument was based on the apparent
impossibility of explaining how the human brain could ever be able to
instantly recall memories, if memories are stored in particular
locations in the brain, because there would be no way for the brain
to know or figure out where a memory was stored. The third argument
was based on the fact that humans can remember 50-year old memories,
but scientists have no plausible explanation for how the human brain
can store memories for longer than a single year.
No doubt some
counterarguments arose in the minds of some readers, particularly any
readers prone toward neural reductionism (the idea that human mental
experiences can be entirely explained by the brain). In this post I
will rebut such possible counterarguments.
The most obvious
counterargument that one could give would be based on the fact of strokes
and Alzheimer's disease. It can be argued that such afflictions show
that very long-term memories are stored in the brain. But such an
objection can be easily answered.
One way of answering
such an objection is to point out that the evidence on brain damage
and memory problems is very mixed. The physician John Lorber
documented many cases of people whose brain tissue had been largely
destroyed by disease, and found many cases of people whose memory and
intelligence was still good. The operation called a hemispherectomy
is sometimes performed on children, and involves removal of half of
their brain. An article in Scientific American tells us,
“Unbelievably, the surgery has no apparent effect on personality or
memory.”
An even better way
of answering such a counterargument is to point out that we cannot
tell whether Alzheimer's patients or strokes have actually suffered a
loss of memories. For it might be that such patients merely
experience a difficulty in retrieving memories.
Imagine you are used
to visiting cnn.com to get the news each morning. But one day you
turn on your computer and find you can no longer access any
information at cnn.com. Does this prove that the information stored
at cnn.com has been lost? It certainly does not. The problem could
merely be an inability for you to retrieve information at cnn.com,
perhaps because of a bad internet connection. Similarly, if I write
the story of my life, and place it on my bookshelf, I may one day go
blind and be unable to access that information. But the information
is still there on my bookshelf.
In the same vein,
the memories of people with Alzheimer's may be perfectly intact, but
such persons may be merely experiencing some difficulty in retrieving
their memories. There are, in fact,
reports of incidents called terminal lucidity, in which people
suffering from memory loss or dementia suddenly regained their
memories shortly before dying. Such reports tend to support the idea
that memory problems such as Alzheimer's involve difficulties in
retrieving memories rather than the actual destruction of memories
stored in the brain.
There is actually a way in Alzheimer's may argue against the idea that your memories are all stored in your brain. A doctor reports the following:
If your brain cells were the only place your memories were stored, why would you not notice memory loss until 40% or 50% of your brain cells were gone?
There is actually a way in Alzheimer's may argue against the idea that your memories are all stored in your brain. A doctor reports the following:
One
of the big challenges we face with Alzheimer's is that brain cell
destruction begins years or even decades before symptoms emerge. A
person whose disease process starts at age 50 might have memory loss
at 75, but by the time we see the signs, the patient has lost 40 to
50 percent of their brain cells.
If your brain cells were the only place your memories were stored, why would you not notice memory loss until 40% or 50% of your brain cells were gone?
Another way of
rebutting my argument about very-long term memory (and our inability
to explain it) is to do an internet search for “long term memory,”
and then find some biological component I didn't mention (perhaps
some kind of protein), a component that is described as “playing a
role in long-term memory.” You might then argue that I failed to
mention that component, and that maybe that is the secret to very
long-term memory.
But such an approach
would be fallacious. Very confusingly, scientists use the term
“long-term memory” for any memory lasting longer than a day. So
anything at all that affects memories lasting longer than a day may
be described as something that “plays a role” in long-term
memory. In general, such things do nothing to answer the problem of
very long-term memory, the problem of how memories can last for years
or decades. For example, PKM protein molecules have been described
as “playing a role in long-term memory.” But having lifetimes of
less than a month, such molecules cannot explain how the brain could
store memories for years.
Very rarely, it is
suggested that maybe epigenetics can explain long-term memory.
Epigenetics involves the effect of methyl molecules that can attach
themselves to a DNA molecule. To use a rough analogy, we can imagine
a DNA molecule as a protein recipe book, and we can imagine these methyl
molecules as being strips of black electrical tape that block out
certain parts of that book. Another analogy is that they are like
“off” switches for parts of DNA. As these methyl molecules are
very simple molecules, they are quite unsuitable for information
storage use. Also, the methyl molecules attached to a DNA molecule
are not connected to each other. So the methyl molecules involved in
epigenetics lack the two characteristics of synapses that caused
scientist to suspect their involvement in memory: the fact that they
can have different “weights,” and the fact that they are
connected to each other.
Another objection
that can be made is to point out that some scientists have come up
with theories trying to explain how information could be maintained
long-term in synapses. Such theories are sometimes called theories of
“synaptic plasticity maintenance” or “synaptic plasticity
persistence,” although given that they involve attempts to show how
unstable synapses could preserve information indefinitely, it might
be better to call them “magic maintenance” theories. Far from
debunking my objection that molecular turnover should make it
impossible for synapses to maintain memories, such theories actually
show that such an objection is quite weighty, and one that scientists
have taken very seriously.
I can characterize
such theories with an analogy. Let us imagine a young boy whose
mother died a year ago. He comes to a beach where his mother used to
swim, and he sees written in the wet sand a message of love.
Engaging in wishful
thinking, the boy decides that the letters were written by his mother
who died a year ago. When his father points out that this couldn't
be, because letters in wet beach sand don't last, the boy comes up
with an elaborate theory. Perhaps, the boy reasons, his mother hired
some people to constantly preserve the letters she wrote in the sand.
Perhaps, the boy thinks, whenever the words are overwritten by the
high tide, some person hired by his mother makes sure that the letters
are rewritten just as his mother wrote them.
Such a theory –
basically a reality denial mechanism – would be very much like the
attempts that have been made to advance theories by which synapses
could preserve memories even though the protein molecules in synapses
are recreated every few days. Both involve complex speculations
hoping to get us to believe that some information that should be very
short-lived is really very long-lived. The synapse theories in
question – these “magic maintenance” theories – are not any
more believable than the little boy's theory about the sand.
One
such theory is a very sketchy theory of “bistable synaptic weight
states,” which just offers the most fragmentary suggestion of how
some special and very improbable “bistable distribution” setup
might help a little --not very much, and not enough to account for
memories lasting for years. But as this 2015 scientific paper
states, “Despite extensive investigation, empirical evidence of a
bistable distribution of two distinct synaptic weight states has not,
in fact, been obtained.” The theory in question relies on an
assumption of unobserved biochemical positive feedback loops, but one
scientific paper notes that “modeling suggests
that stochastic fluctuations of macromolecule numbers within a small
volume such as a spine head are likely to destabilize steady states
of biochemical positive feedback loops,” making them unsuitable for
anything that can explain long-term memory.
Another
such theory is a “cluster dynamics” theory advanced in this
paper. The author makes a totally unwarranted ad-hoc speculative
assumption. Speaking of the insertion of a new protein – where a
new protein would appear when a brain cell replaces a protein, as it
constantly does – the paper says, “The
primary effect of this implementation is that the insertion
probability at a site
with many neighbors (within a cluster or on its boundary) is orders
of magnitude higher than for a site with a small number
of neighbors.” There is no reason for thinking that there should be
any difference in these probabilities. He then attempts to show that
this imagined effect can work to preserve the information in
synapses, by giving us a “simplest possible case” example of a
square shape that is preserved on a grid, despite turnover of its
parts. But
such an effect would not work in cases much more complicated than
this “simplest possible” case, and would not work to preserve
information more complicated than a square.
I tried created a
spreadsheet that would use this type of effect. After a great deal of
trial and error, I was able to find an “intensity of neighbors”
formula that would set things up so that the lower set of numbers in
the photo below (marked Generation 2) recreates the data in the first
set of numbers (marked Generation 1). The formula used to create
Generation 2 used the same idea in the “cluster dynamics” theory
– the value of an item in the second generation depends on how high
are the nearby values in the earlier generation. When I tried using some square-shaped data in
the Generation 1 area, the effect worked okay, and the Generation 2
area looked like the Generation 1 area.
But as soon as I
tried using some data in the Generation 1 area that was not
square-shaped (such as X-shaped data or E-shaped data), the effect no
longer worked. Here are the results when you try some E-shaped data.
The resulting Generation 2 does not look like an E-shape.
Simple as this
experiment was, it captures the fatal flaw of this “cluster
dynamics” theory. While it might work to explain a preservation of
the simplest possible data (square shapes), it will not work to
preserve any data more complicated, such as E-shapes and X-shapes. Of
course, our memories involve memories of things infinitely more
complicated than an X shape.
All of these
“synaptic plasticity maintenance” theories have one thing in
common: they have already been ruled out by experiments with
long-term potentiation (LTP) and synapses. Such experiments have
shown that LTP very rapidly degrades, and that synapses do not
magically maintain their information states over long periods.
Another objection
that could be made is one along these lines: sure, scientists don't
have an explanation now for very long-term memory, but they'll find
out someday how the brain is storing it. My answer to this is: no,
they won't, because there are good reasons for thinking there is no
place where it could be stored in the brain. The only candidates for
places where very long-term memory could be stored in the brain are:
synapses, DNA in nerve cells, protein molecules surrounding the DNA,
other nerve cell proteins, or what is called the perineuronal net. My
previous post made a good case that none of these are plausible
storage places for very long-term memory. If you've ruled out all
the places where something could be in some unit of space, then you
have to conclude it's not in that space. For example, if you're
looking for your car keys and you've ruled out all the places they
might be in your bedroom, you should conclude they are not in your
bedroom (rather than telling yourself: I'll find them some day hidden
in my bedroom).
What
is very astonishing is the difference between the longest memory that
can be plausibly explained by neuroscience, and the longest memory that humans
can hold. As discussed in my previous post, the best “candidate
explanation” for memory is LTP (long-term potentiation), but that
decays in a matter of days. The protein molecules between synapses
also last no longer than two weeks. Even if you were to claim that
LTP is a good mechanism for memory (something quite questionable,
since it doesn't correlate highly with memory), then about the
longest memory that science can currently explain (without resorting to baroque speculation) is a memory lasting
about two
weeks.
Because humans can hold memories for 50 years, they are displaying a
memory capacity that is about 1000 times longer than what can be
plausibly explained by neuroscience. The explanatory gap here is
like the gap between Jupiter and Saturn. How long will it be until we
wake up, smell the coffee, and realize that to explain our minds we
must go beyond the brain?
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