Why Strokes, Alzheimer's Disease and Drunkenness Don't Prove the “Brains Make Minds” Dogma

A person believing that brains generate minds may refer us to cases of Alzheimer's disease, and say this proves this brains make minds and store memories. Or the person may make a similar argument when referring to strokes. Or the person may claim that drunkenness shows your brain makes your mind, because in that we see a physical liquid causing a judgment deterioration. In this post I will address these objections.

Alzheimer's disease could never prove that brains make minds, because we do not see in Alzheimer's disease an actual loss of the self or consciousness.  A mind with very poor memory is still a mind.

In regard to Alzheimer's disease or strokes, we cannot actually tell whether a person has 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:

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 place your memories were stored, why would you not notice memory loss until 40% or 50% of your brain cells were gone?

The evidence in regard to the cause of Alzheimer's diseases is actually pretty baffling. The most common explanation is that the disease is caused by something called amyloid plaques. But the Chicago Tribune tells us, “Scientists have learned that about a third of people who appear to have Alzheimer's disease do not have high levels of amyloid in their brains.”

A brain study was made of nine very old people who scored particularly high on a memory test. After these people died, their brains were examined. Three of the nine very old “super memory” people were found to have brains filled with the plaques often seen in Alzheimer's patients. These “super memory” people had brains in much worse shape than a large fraction of Alzheimer's patients with very poor memories.

In 2017 there was a news story entitled, "New Discovery Suggests Neuron Death Does Not Kickstart Dementia." The story reported this:

The leading theory in Alzheimer’s disease is that memory loss is the result of neuron death and nerve ending damage, which lead to memory loss, are caused by the formation of toxic protein clumps in the brain, called tau tangles and beta-amyloid plaques. But a new, small study challenges this theory, showing that the loss of neurons in brains of people with dementia is actually very small. What’s more, levels of neuron loss in patients did not indicate how far along the were in the disease, suggesting neuron death has little to do with the symptoms of dementia. 

The news story quotes a scientist saying the following:

Much to our surprise, in studying the fate of eight neuronal and synaptic markers in our subjects’ prefrontal cortices, we only observed very minor neuronal and synaptic losses. Our study therefore suggests that, contrary to what was believed, neuronal and synaptic loss is relatively limited in Alzheimer’s disease. 

A book on dementia says on page 34 that in the pioneering Blessed, Tomlinson and Roth study (1968) "there is only a rather low correlation between the brain plaque count and the test scores among the senile" -- not what we would expect if brain plaques were causing memory loss.  There were four cases with a high plaque count and low dementia. The book tells us that in a well-known study involving nuns and Alzheimer's disease, one of the nuns had high cognitive scores despite having "abundant neurofibrillary tangles and senile plaques." The book tells us that "predicting backwards from autopsy to clinical diagnosis appears unreliable and poorly predictive," which is not what we would expect if dementia was really caused by brain states. 

After telling us on page 35 that "there are many reports of people carefully diagnosed...as clearly having the clinical symptoms of dementia and yet showing no evidence of brain pathology,"  the book gives this quote from a neuroscientist named Robert Terry:

Over the years, investigators have sought assiduously for lesions or tissue alterations in the Alzheimer's brain which...might at least correlate with clinical determinants of the disease severity....Despite 30 years of such efforts, clinico-pathologic correlations have been so weak or entirely lacking that determination of the proximate, let alone the ultimate, cause of Alzheimer's disease (AD) has not been possible. 

The scientific paper here made an examination of 14 brains of recently deceased people who had donated their brains to medical science. Four were controls, five were people with Alzheimer's disease but no dementia, and five were people with Alzheimer's and dementia. The paper made detailed comparisons of the number of neurons in the brains and the total number of cells in the brains as a whole. The "bottom line" of the study is in Figure 6, which is below. The white bars are the controls; the gray bars are those with asymptomatic Alzheimer's; the black bars are those with Alzheimer's and dementia. 

We see here nothing to back up common claims that Alzheimer's is some disease that robs people of large number of neurons. The number of neurons is about the same for all three groups, and the total number of cells is greater for those with Alzheimer's.  Such a study shows that a common visual (showing a normal brain side- by- side with a shrunken Alzheimer's brain) is misleading, and that the idea of very large neuron loss as a hallmark of Alzheimer's is incorrect. 

The 2009 study "Comparison of Different MRI Brain Atrophy Rate Measures with Clinical Disease Progression in AD" compared brain shrinkage in 55 normal people and 64 people with Alzheimer's disease.  In Table 2 we see that 40 of the normal people had whole brain shrinkage of 0.4 % per year, and 15 of the normal people had whole brain shrinkage of 0.8 % per year.  For those with Alzheimer's disease, 32 had whole brain shrinkage of 0.6 % per year (less than 1% per year), and that 33 had whole brain shrinkage of 1.4% per year.  In short, there was hardly any difference between the brain shrinkage rates for those with Alzheimer's and the normal people.  The 2019 paper "Lifespan Changes of the Human Brain In Alzheimer’s Disease" presents a model based on brain scans of hundreds of healthy controls and hundreds of people with Alzheimer's disease. Figure 1 of the paper depicts the lifespan changes of white matter and gray matter of those with Alzheimer's disease and normal healthy people. The lines look almost identical. 

Given these conflicting findings, it seems that the evidence is not telling us any clear tale in regard to what causes Alzheimer's. Very many of the people with Alzheimer's have amyloid plaques in the brains, but one third do not. And apparently lots of people with very good memories have amyloid plaques, and many do not. There is also no strong correlation between neuron loss and dementia. Such evidence gives us no clear signal as to whether our memories are stored in our brains.

As for strokes, they can damage an ability to move, speak or understand language. Understanding language is partially based on auditory processing, and speaking language is based on muscular finesse in the vicinity of the tongue and vocal chords. We know that the brain helps the senses do their work, and is involved in muscular control. But an article in US News and World Report says, "It’s important to recognize that strokes do not cause a drop in overall intelligence.” On quora.com, someone states, "My speech therapist was pretty adamant that having a stroke does NOT, in any way, affect your intelligence." That's something we would not expect under the theory that the brain generates the mind. Under that theory, we might expect that people would lose half or more of their intelligence after a stroke.

If our memories were stored in our brains, what we would expect is that people would often get amnesia after a stroke. But such a thing seems to happen only very rarely.  A scientific paper says, "Reports of amnesic syndrome due to unilateral stroke have appeared infrequently." The paper lists some new cases which it claims are new examples, but when we read the examples we find typically only mild things like an inability to recall a daughter's phone number. Speaking of strokes, the paper says, "There have been two reported cases of persistent amnesia following unlitateral infarctions in which there were no other neurological deficits," indicating the rarity of such a thing. The paper also says that of a group of 68 patients who had brain infarctions, there were no cases of amnesia.  Talking about strokes, this paper says, "Amnesia as the main symptom of acute ischemic cerebral events is rare, mostly transient, and easily mistaken for TGA [ transient global amnesia]." 

What about drunkenness? Does drinking alcohol really cause you to “lose your mind”? Not really.

Consider the case of the drunk asked to walk a straight or to touch his finger to his nose. If such a person really had his mind dulled by the alcohol, he would be unable to interpret the police officer's language. But instead such a drunk will normally understand the command just fine, and attempt to follow it.

What we mainly see in drunkenness is a kind of overconfidence and loss of inhibition, along with mood changes and a deterioration of muscle skills. You don't really see people losing their minds or memories while they are drunk. If they did, they would probably forget how to start up their cars (or do something like putting their combs or their fingers in the ignition slot rather than their keys).

A CBS New story says that people who consumed alcohol were actually better at certain creative problems.

In fact, there is no such thing as a “temporary stupid potion” that will cause an intelligent person to regress to the intelligence level of a small child, nor is there any such thing as a “temporary amnesia potion” that will cause you to forget where you grew up or where you live or what your mother's name is. Wikipedia.org has an article on “drug induced amnesia,” but gives us no examples of any such drug other than benzodiazepines (which do not produce retrograde amnesia, the inability to recall old memories) but only help produce antograde amnesia (the inability to make new memories).

But if your memories do actually come from your brain, and your intelligence comes from your brain, we would think that such potions should have been invented already. If your memories do actually come from your brain, and your intelligence comes from your brain, it should have been easy for scientists to create some potion that would temporarily disrupt the chemistry supposedly needed for memory recall and thinking. The nonexistence of any such potion is actually further evidence against the claim that your brain is the source of your thoughts and the storage place of your memories.

Postscript: A recent study (which found no correlation between the number of neurons in the brains of 50 subjects and their IQs) refers to the fact "that highly demented female Alzheimer’s disease patients have normal neocortical neuron numbers (Regeur et al. 1994, Pelvig et al. 2003)`"

Against the objections of its advisory Peripheral and Central Nervous System Drugs Advisory Committee, the FDA approved not long ago a drug for Alzheimer's, the first such drug to be approved since 2003. The drug is fantastically expensive, costing more than $50,000 per year, and there is no compelling evidence that it works. People are arguing that it "provides hope for families," but so would a placebo pill, which would be very inexpensive.  In early 2024 we heard that Biogen is abandoning the drug, apparently because of its low effectiveness. 

Some studies (mostly with small study group sizes such as about 25) have claimed to find smaller volumes in the hippocampus of those with Alzheimer's, with such people having perhaps 15% smaller hippocampus volume. Such studies are problematic partially because of the small number of subjects and also because of the small volume of the hippocampus, which is only about 1/400 (one four-hundredth) the size of the brain. A 2016 study has the title "

No Association of Lower Hippocampal Volume With Alzheimer’s Disease Pathology in Late-Life Depression." It involved more than 50 patients and 50 controls. In a section entitled "Associations between clinical factors, hippocampal volume, and amyloid binding in patients," we read that "No main effects were detected for measures of episodic memory, including total learning, delayed recall, and delayed recognition." The largest study of hippocampal volume is the study here, involving 19,000 people, and showing a decline from about 8000 cubic millimeters at age 50 to about 7200 cubic millimeters at age 75. 

A 2023 press release on a study  tells us that "a University of California, Irvine-led team of researchers have discovered that the oldest-old, those who live to be 90+ and have superior cognitive skills, have similar levels of brain pathology as Alzheimer’s patients." The study is  the paper here entitled "A Population-Based Clinicopathological Study in the Oldest-Old: The 90+ Study." We read this:

"Half of all non-demented participants (49%) and just over half of demented participants (57%) met pathological criteria for AD [Alzheimer's Disease], ... The pathologies examined to date failed to explain all dementia in this cohort, as almost one quarter (22%) of all demented participants did not have significant AD or any other pathology to explain their cognitive loss."

The visual below has a graph from the paper:

Another recent study tells us the number of people with Alzheimer's Disease and the typical brain pathology claimed to cause that disease is even less than the 57% depicted in the graph above, and also tells us that some things described as causes of dementia are found in almost all who died without ever having dementia.. In the study  we read this:

"Pure AD [Alzheimer's Disease] neuropathology is observed in less than half of patients diagnosed with probable AD dementia in life... Some level of AD pathology has also been observed in nearly 40% of dementia patients, who were considered to have non-AD diagnoses during life. Moreover, many elderly individuals considered cognitively normal proximate to the time of death have been demonstrated to have AD pathology at autopsy.....Boyle et al. [90] reported that among 467 individuals who had been studied longitudinally and remained non-demented till autopsy, the vast majority had beta-amyloid, all had tangles, about a quarter had macroscopic infarcts, another quarter had microinfarcts, and between 5 and 10% had neocortical Lewy bodies."

The paper also tells us the following, which doesn't sound like what we would find if the cause of dementia was mainly physical: "Among a cohort of over 1000 elderly individuals without dementia at baseline, followed for an average of 12 years, the rate of global cognitive decline in five domains of cognitive function was reduced by an average of 70% in persons who were at the 90th percentile of social activity, compared to persons who were at the 10th percentile." 

An excellent paper on this topic is the paper "Exploring why 'memory loss' is a misleading descriptor of people living with dementia and can lead to dysfunctional care" by Steven R. Sabat and Alison Warren. The paper points out that there are many types of memory and aspects of memory, and that it is misleading to be using the term "memory loss" for someone who has difficulty with one aspect of memory but who may still have other aspects of memory. We read this:

"Explicit episodic memory is the type of memory most affected by the disease process of AD [Alzheimer's disease], but implicit memory types are relatively spared and can contribute to familiarity that informs recognition (Deason et al., 2019). Explicit and implicit memory are only two of many types of memory. Not only are there several types of memory systems (i.e., short-term; working; long-term; declarative/explicit; nondeclarative/implicit; autobiographical; episodic; emotional, etc.), but also different ways in which they interact in the daily milieu of human existence (Poldrack et al., 2001). ... Remarkably, there have been observations of significant lucidity despite an advanced stage of disease (Griffin et al., 2022; Mashour et al., 2019; Ramirez et al., 2023). The salient concept is that the severity of memory problems, or likewise, the ability to retrieve information from memory, fluctuates greatly. Indeed, persons with dementia have memory difficulties, but to say they have memory loss is clinically inaccurate. Furthermore, the memory difficulties that manifest can vary by dementia type. For example, a person with AD may have difficulty with episodic memory of events and personal experiences, but maintain procedural memory (learned skills, habits) (Kudlicka et al., 2019), while other forms of dementia,...affect memory quite sparingly and instead result in visual deficits (Crutch et al., 2012; DeTure & Dickson, 2019). Regardless of the type of dementia, it has long been known, but rarely discussed, that persons with dementia retain considerable cognitive capacities and are capable of new learning (Kudlicka et al., 2019). For example, studies examining cognitive plasticity and learning potential in persons with MCI and AD have demonstrated improved performance in visual memory, verbal learning, and executive function in all participants (Backman, 1992; Fernandez-Ballesteros et al., 2006), challenging the enduring notion that persons with dementia lose their memory but are also incapable of creating new memories. In addition to the preservation of implicit memory in general, persons with dementia maintain other components under this classification, including emotional memory, emotional communications, a variety of skills, and ability to learn....Furthermore, research supports that even during cognitive decline, persons with cognitive impairments can continue to learn new skills and thus create new memories (Sabat, 2018). Considering the evidence, dementia is a syndrome of memory retrieval difficulties rather than loss and characterizing it as such can have far reaching consequences for persons with dementia, especially how they are treated and the fate of their quality of life."

A paper states this:

"Patients with the same neurological disease and comparable brain damage often display different functional outcomes. For example, more than 25% of elderly individuals with no sign of cognitive impairment met post-mortem pathological criteria of Alzheimer’s disease (AD).1 By the same token, 10–40% of individuals with mild to moderate brain pathology showed no clinical symptoms of dementia."