By 2050, worldwide Alzheimer’s cases may quadruple

From a recent AP news article: “More than 26 million people worldwide have Alzheimer’s disease, and a new forecast says the number will quadruple by 2050. At that rate, one in 85 people will have the brain-destroying disease in 40 years, researchers from Johns Hopkins University conclude.”

It’s had to imagine the costs on society that this will have – 100 million people in the world with Alzheimer’s! It could be devastating both emotionally and financially.Old Man

Alzheimer’s disease (AD) has an estimated yearly associated cost in the United States of $100 million (US). This cost results from direct care, lost wages of care takers, and so forth. AD is turning into quite an epidemic; hopefully researchers can find a cure for this debilitating disease. One book that I’ve enjoyed tremendously about AD is Learning to Speak Alzheimer’s by Joanne Coste (available from Amazon for around $10 US). It is easy to read and written with great compassion by someone who truly does understand Alzheimer’s disease.

War-related traumatic brain injuries

An article in the most recent Monitor on Psychology (published by the American Psychological Association) [here’s a link to the article that is accessible for free online: Link) reminded me of something one of my professors in graduate school told our class a couple years ago. He is a clinical neuropsychologist who occasionally does some consulting for the military. After he returned from a consultation with the military he told us that between the war in Afghanistan and the Iraq war there had been 18,000 central nervous system (brain and spinal cord) injuries of soldiers and contract employees serving in those two countries. The majority of the injuries were minor and many were not combat related but there are still thousands of people with moderate to severe CNS injuries that were acquired in war zones. Quoting from the Monitor article:

“Psychologists, particularly neuropsychologists, are stepping in to assess the damage, help patients learn new strategies to compensate while their brains recover, and raise public awareness of the increasing number of servicemen and women with TBIs. In fact, 1,977 service members were treated for them at Defense and Veterans Brain Injury Center (DVBIC) sites from January 2003 to February 2007.”Soldier Helmet

One reason for high rates of traumatic brain injury in the Iraq (and Afghanistan) war(s) is the improved (compared to previous wars) body armor and other life-saving devices. The downside to fewer fatalities is that there are higher rates of people with severe injuries who survive. The mild TBI rates are shown to be: “between 10 and 20 percent [in some surveys] of soldiers returning from deployments” (Source). It’s great to have fewer fatalities but TBIs can have profound effects on people. Clinical neuropsychologists can help people with TBIs learn how to best cope with their injuries as well as understand how their lives might be different and what they can do to compensate for any difficulties. Most people with mild to moderate TBIs seem to have complete or nearly complete recoveries; however, those with moderate to severe TBIs may have deficits, many very severe, that last the rest of their lives.

There can be myriad short-term problems associated with TBIs (e.g., mental slowing, memory problems, personality changes, concentration and attentional difficulties, etc.) but there are also long-term ones. Research has shown that a person with a history of multiple TBIs is more likely to get Alzheimer’s Disease in old age (well, the research actually shows that there is an over-representation of people with multiple TBIs in the Alzheimer’s population). There is a great need for clinical neuropsychologists currently and in the future to work with and help all of our war veterans who have acquired brain injuries.

Motor learning – It’s good being in the background

This was a story I first saw on Digg today but it’s worth posting about here. Researchers at MIT recently published a study in Neuron (May 24, 2007 issue) that demonstrates a completely new way of looking at motor learning. From their article:

“In experiments on motor learning, it is often assumed that there is an underlying neural representation that is stable and that adaptation takes place on top of this stable background. Our experimental and theoretical results suggest a radically different picture. The experiments show that tuning curves of motor cortical cells are constantly changing even when performing a familiar task. Furthermore, when learning a new task, learning-related changes occur on top of this background of changing tuning curves” (Rokni, Richardson, Bizzi, & Seung, 2007, p. 661).learning_theory.jpg

They are proposing that the neuronal activity associated with motor learning is a little like a sail-less ship on the ocean. This ship not only goes up and down the waves as they come, it also drifts about somewhat randomly in response to the underlying and unstable movement of the water underneath. This analogy isn’t perfect but it is OK.

Learning is not only a component of the active responsive brain activity but also the somewhat random low-level “background noise” that is slowly “retuned” and “retunes” in response to motor learning. This background noise only affects the synapses very slowly but it has a noticeable effect: “According to our theory, this slowness is necessary to prevent the noise from erasing motor memories” (p. 663). They do believe that this unstable foundation for learning is linked to forgetting over time. The researchers also state that there may be many ways that neurons can represent essentially the same behavior: “any single behavior can be realized by multiple configurations of synaptic strengths” (p. 653).

Anyway, the article was an interesting read and well worth the time if you have any interest in cognitive psychology. [The posted image is directly from the article in Neuron and is ©2007 Elsevier Inc].


Rokni, U., Richardson, A. G., Bizzi, E., & Seung, H. S. (2007). Motor learning with unstable
neural representations. Neuron, 54, 653-666.

Acute Respiratory Distress Syndrome

Acute respiratory distress syndrome is a common cause of mortality and morbidity, affecting an estimated 150,000 people per year in the United States (Rubenfeld, Doyle, & Matthay, 1995) however, recent evidence suggests the incidence may be higher (Rubenfeld, 2003). Compared to 20 years ago mortality has decreased from 80% to 30% of ARDS participants (Milberg, Davis, Steinberg, & Hudson, 1995; Brower et al., 2000) resulting in approximately 100,000 people who survive ARDS each year in the United States (Bersten, Edibam, Hunt, & Moran, 2002). Acute respiratory distress syndrome occurs in response to a variety of insults including sepsis, trauma, pneumonia, massive transfusion and other medical/surgical conditions. Treatment of ARDS requires aggressive supportive care including positive pressure ventilation (Brower et al., 2000) and increased oxygen concentrations with risks of barotrauma, oxygen toxicity, and nosocomial infection.

Acute respiratory distress syndrome may be a consequence of multiple organ system dysfunction, including the central nervous system (Bell, Coalson, Smith, & Johanson, 1983; Montgomery, Stager, Carrico, & Hudson, 1985). Participants who survive ARDS are at risk for neuropsychological deficits (Hopkins et al., 1999; Rothenhausler, Ehrentraut, Schelling, & Kapfhammer, 2001; Al-Saidi et al., 2003; Hopkins, Weaver, Chan, & Orme, 2004) 6 to 12 months following hospital discharge. Approximately 33% of general medical ICU survivors, some with ARDS, have cognitive impairments (Jackson et al., 2003) 6 months after hospital discharge. In 1999, Hopkins and colleagues found that 45% of ARDS survivors had neurocognitive impairments including impaired memory, attention, concentration, mental processing speed, and global intellectual decline one year post-discharge.

Others have since made similar observations (Marquis et al. 2000; Rothenhausler et al., 2001; Al-Saidi et al., 2003; Jackson et al., 2003). The prevalence of neurocognitive impairments varies from 25% (Rothenhausler et al., 2001) to 78% in participants with more severe ARDS (Hopkins et al., 1999). Neurocognitive impairments are a major determinant in return to work, work productivity, and life satisfaction following ARDS (Rothenhausler et al., 2001).


Al-Saidi, F., McAndrews, M. P., Cheunt, A. M., Tansey, C. M., Matte-Martyn, A., Diaz-Granados, N., et al. (2003). Neuropsychological sequelae in ARDS survivors. American Journal of Respiratory and Critical Care Medicine, 167, A737.

Bell, R. C., Coalson, J. J., Smith, J. D., & Johanson, W. G., Jr. (1983). Multiple organ system failure and infection in adult respiratory distress syndrome. Annals of Internal Medicine, 99, 293–298.

Bersten, A. D., Edibam, C., Hunt, T., & Moran, J. (2002). Incidence and mortality of acute lung injury and the acute respiratory distress syndrome in three Australian States. American Journal of Respiratory and Critical Care Medicine, 165, 443–448.

Brower, R. G., Matthay, M. A., Morris, A., Schoenfeld, D., Thompson, B. T., & Wheeler, A. (2000). Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. New England Journal of Medicine, 342, 1301–1308.

Hopkins, R. O., Weaver, L. K., Chan, K. J., & Orme, J. F. (2004). Quality of life, emotional, and cognitive function following acute respiratory distress syndrome. Journal of the International Neuropsychological Society, 10, 1005–1017.

Hopkins, R. O., Weaver, L. K., Pope, D., Orme, J. F., Bigler, E. D., & Larson-Lohr, V. (1999). Neuropsychological sequelae and impaired health status in survivors of severe acute respiratory distress syndrome. American Journal of Respiratory and Critical Care Medicine, 160, 50–56.

Jackson, J. C., Hart, R. P., Gordon, S. M., Shintani, A., Truman, B., May, L., et al. (2003). Six-month neuropsychological outcome of medical intensive care unit participants. Critical Care Medicine, 31, 1226–1234.

Marquis, K., Curtis, J., Caldwell, E., Davidson, T., Davis, J., Sanchez, P., et al. (2000). Neuropsychological sequelae in survivors of ARDS compared with critically ill control participants. American Journal of Respiratory and Critical Care Medicine, 161, A383.

Milberg, J. A., Davis, D. R., Steinberg, K. P., & Hudson, L. D. (1995). Improved survival of participants with acute respiratory distress syndrome (ARDS): 1983-1993. Journal of the American Medical Association, 273, 306–309.

Montgomery, A. B., Stager, M. A., Carrico, C. J., & Hudson, L. D. (1985). Causes of mortality in participants with the adult respiratory distress syndrome. American Review of Respiratory Disease, 132, 485–489.

Rothenhausler, H. B., Ehrentraut, S., Stoll, C., Schelling, G., & Kapfhammer, H. P. (2001). The relationship between cognitive performance and employment and health status in long-term survivors of the acute respiratory distress syndrome: Results of an exploratory study. General Hospital Psychiatry, 23, 90–96.

Rubenfeld, G. D. (2003). Epidemiology of acute lung injury. Critical Care Medicine, 31, S276–S284.

Rubenfeld, G. D., Doyle, R. L., & Matthay, M. A. (1995). Evaluation of definitions of ARDS. American Journal of Respiratory and Critical Care Medicine, 151, 1270–1271.

Brain Injury Video

Here’s a decent video about brain injury that does a good job of showing how brain injury affects people.

Unfortunately, we don’t have the ability to completely reverse the effects of acquired brain injury. Therapy and rehabilitation can help but if the injuries are severe, completely normal functioning is unlikely ever to return. Prevention is the best medicine in this case; it is unfortunate that prevention is not always possible.The parts of the brain that are most often affected with brain injury are those that have to do with memory.

Another common outcome of brain injury is cognitive slowing – people just don’t seem to think or move or act as quickly after brain injury as they did before. This slowing is due in part to the diffuse axonal injury that occurs (the connections between brain cells {neurons} are broken or twisted as the brain compresses and stretches) with traumatic brain injuries. Even non traumatic brain injuries (e.g., carbon monoxide poisoning) can result in overall cognitive slowing (this slowing often greatly improves over time with mild to moderate brain injuries).It is also fairly common to see personality changes in someone with a recent brain injury – this is mainly due to damage to the frontal lobes. These changes in personality can be the source of great frustration and concern for family, friends, and everyone around the injured person. Dealing with a severe brain injury requires a lot of loving, patience, and care.

Recent alcohol research


There was an interesting recent news story from Reuters. Researchers at the University of Missouri-Columbia found that, “Young adults who binge drink frequently are more likely to show disadvantageous decision-making patterns than their peers who don’t drink as heavily” (from the news article). You can’t assume that just because drinking and poor decision making are correlated that the drinking causes the poor decisions (because people who are poorer at decision making in general may drink more) but as I like to say, “Correlation does not imply causation but neither does does it deny causation.”

On the other hand, there is some evidence that drinking alcohol might slow down the progression and/or onset of dementia (e.g., Alzheimer’s Disease): Alcohol and dementia article. Again, the study is correlational so firm causations should not be inferred.

These two articles demonstrate that there is still a lot of  uncertainty about the long-term effects of alcohol consumption.

Human brain development

The brain is a magnificent organ. It is the reason humans spend 9 months in utero – to give the brain time to develop sufficiently. Human infants could even spend more time in the womb but due to birth canal size restraints, 9 months of development and head growth is all that mothers can handle. The human brain at birth has an over-abundance of neurons. Within the first 2 years of life, the brain prunes back the number of neurons as they are unneeded. Even in adulthood the number of neurons in the Central Nervous System (brain and spinal cord) is astounding – estimated at 100 billion! The number of connections between neurons – composed of dendrites, axons, and synapses – is estimated at 100 trillion.

At birth, few areas of the brain are well-myelinated. Myelin is a largely lipid-based substance (part of a type of glial cell; glial cells serve in mainly supportive roles to neurons) that wraps around the axons of neurons, like insulation around electrical wires, which increases the speed of transmission of action potentials – electrical impulses that travel down the axon when the signal is outgoing (or down the dendrites if the action potential is incoming). Myelination of the brain is not complete until into a person’s third decade of life, with the frontal lobes being myelinated last. The frontal lobes provide a lot of the oversight and control of the brain – decision making, language, and problem solving – so this slowness to myelinate in part explains children’s and adolescents’ often less-than-ideal reasoning (not that adults have wonderful reasoning all the time but adults often are more likely to think things through and be able to reason with complexity about situations and ideas).

So, the brain is such a complex and marvelous organ that it is a wonder that it develops so well most of the time.

Neuroimaging and Image Analysis

A handy program I use to analyze MRI data is called FSL. “FSL is a comprehensive library of image analysis and statistical tools for FMRI, MRI and DTI brain imaging data. FSL is written mainly by members of the Analysis Group, FMRIB, Oxford, UK” (from the FSL website). It is powerful, flexible, and well-maintained. There is a very active community listserv too.

All of my research is structural MRI-based, so the main FSL tools I use are: Brain Extraction tool (BET), SUSAN (which reduces noise nonlinearly), FAST (an automated segmentation program that can separate the MR images into different tissue types), FLIRT (a linear registration program), and FUGUE (a program that can unwarp the MR images; there is often distortion in MRIs caused at scan acquisition by head movements or other problems).

I’ve been very pleased with the software so far. It’s free software and available to pretty much anyone for use. I have no affiliation with the software developers, I am just a pleased user of the software. I would post some of the images I’ve processed with FSL, however, due to IRB, HIPPA, and confidentiality limitations, I am unable to.

Anosognosia and Dementia

Anosognosia is a word that means unawareness of functional deficit. It is a common condition in people with Alzheimer’s Disease (AD) – they are not fully aware of their deficits. We can’t state that people with AD never have awareness of their deficits because there is a fair amount of evidence that in the earlier stages of AD there is at least some awareness of memory problems and slowed cognition. The relative anosognosia in AD patients can be contrasted with Parkinson’s patients who are all too aware of their deficits. Theirs is mainly a motoric disorder, which is brought about by neuronal death in the substantia nigra, an area of the brain that produces dopamine (a neurotransmitter). The resting tremors and slowed movements can been extremely frustrating to people with Parkinson’s disease because they are completely aware of their problems.

On Alzheimer’s Disease and other dementias

There are two general classes of dementias: cortical and subcortical. A cortical dementia is one like Alzheimer’s Disease (AD) where the outer layer (the “bark”) of the brain is first affected. AD typically affects the ventromedial frontal and dorsomedial temporal lobes first. The medial portions of the temporal lobes (e.g., hippocampus and parahippocampal gyrus) are heavily involved in memory processes. So typically with AD we first see atrophy (or volume loss) in those regions; the gray matter (bodies of neurons) die off and the brain shrinks. We are still not entirely sure what causes AD – we know genetics plays a part as do environmental factors such as exercise, nutrition, and education but we don’t know the specific pathology of the disease. AD also is related to swelling to some degree; so an adult who is approaching old age can likely reduce the chances of getting AD simply by taking a “baby aspirin” daily. At the very least it will likely delay the onset and slow down the progression of the disease.

There are also subcortical dementias. These can occur as a result of stroke, Huntington’s disease, or Parkinson’s disease. These types of dementias can occur and worsen rapidly (in the case of strokes) or can be fairly mild initially (as in Parkinson’s-type dementias). Subcortical dementias will over time and in the latest stages of the disease become indistinguishable from AD. Another type of subcortical dementia is Dementia with Lewy Bodies (DLB, or Lewy-body dementia). This is a disease that appears to combine aspects of Parkinson’s, Alzheimer’s, and schizophrenia. People with DLB often have vivid visual hallucinations and other psychoses. It is a terrible disease for the person with it as well as caretakers and family.