Age and Brain Change - Understanding and Preventing Dementia
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Amazing improvements in imaging techniques are giving us new insight into the mechanics of the brain and its malfunction in dementia. A typical CAT scan (computed tomography scan) and MRI (magnetic resonance imaging) can vaguely depict changes in brain volume, stroke damage, and other structural areas that may identify dementia. One PET imaging scan (positron emission tomography) will actually render the presence of protein plaques associated with Alzheimer’s dementia. Another new imaging technique, DTI (Diffusion Tensor Imaging) can represent the input and output fibers that connect different parts of the brain. These whitematter fibers precisely coordinate information processing with signals from higher and lower systems and different sensory modalities and related memories. Any disruption along a network pathway may impact related abilities from connected regions. Thus one damaged area may impact functions from a different cortical or subcortical area that is linked to the blighted site. Maladies of these important brain fiber connections are usually called white matter deficits.

The composition and connectivity of each brain system is reflected in symptoms of malfunction that occur in dementia. Take Parkinson’s for instance. This Disease is associated with progressive declines in attention, complex thinking, and movement disorders that are related to deficits in the dopamine system, which has input and output to areas primarily involving decision-making, movement and pleasure. Thus Parkinson’s patients experience a progressive decline in these linked brain regions.

The dementia research, mostly coming out of progress in brain and molecular imaging, is leading to an understanding of brain function from a perspective of a network model. Because of this brain researchers are beginning to think of different areas of the brain and their associated functions as simply primary nodes on networks that connect one system to another related one. Through evolution the brain expanded with new complex thinking areas superimposed over old subcortical areas that are related to heart rate, sensation, movement, etc. The lower areas reacted to the newer areas by elaborating their own networks to the newer brain parts so as to more efficiently coordinate responsivity across systems and sensory modalities. For example the emotional system has connections to lower subsystems that are related to respiration, blood pressure, movement, etc. and also to higher systems that control decision-making, judgment and self-awareness.

Combining information from several imaging techniques has revealed that the brain has a default network signal pathway that oscillates predictably when an individual is in a quiet, resting state. This default-signaling network is suspended when the resting individual is activated during intentional behaviors, such as purposeful movement, learning or social interaction. The resting state pattern returns when behavior is quiet. Resting pattern signals reflect basic underlying organizational properties of the human nervous system. Could this be why so many people try to self regulate, “find centeredness,” though meditation or other behaviors that result in a return to our sense of a quiet peaceful state? This new information about a default brain resting state certainly implies that our body naturally seeks a state of balance and quiet. The brain clearly needs tranquil awake time on an ongoing basis to preserve its durability.

We know now that behavioral, cognitive and psychological symptoms in all dementias are related to the areas and fiber network connections that are pathologically impacted. The configurations of the imaged pathological changes may help to delineate the kind of dementia that is in progress. For instance, dementias related to addiction have underlying damage in circuitry in the prefrontal cortex and connections to other brain regions such as the cerebellum. This damage results in symptoms of disinhibition, poor judgment, irritability, and impulsivity because the connected areas relate to these abilities.

In addition to our ability to better diagnose previously known types of dementia, we have recently been able to distinguish what is called Frontal Lobe Dysfunction (FTD), which involves neurodegeneration primarily within the front of the brain. Symptoms include impaired judgment planning and insight, self-regulation, motivation and initiative, and the inability to appreciate consequences of behavior. As a result, FTD is now being diagnosed earlier. Because often the family or spouse is first aware of subtle initial changes and because of the specificity of these changes, neurologists are recommending that they participate in reviewing the actual scan of the brain, rather than having a radiologist alone compose the diagnostic report.

Alzheimer’s disease, along with some of the other dementias, is associated with a mutated protein synthesis in the brain that may be both genetic and environmental in origin. At a molecular level we can see cellular changes in dementia showing deposits and tangles that differ from normal. For example, the brain tissue in Parkinson’s dementia typically exhibits Lewy bodies, which are small, diffuse microscopic abnormalities that are distinctive from the microscopic abnormalities seen in Alzheimer’s disease.

While there are recent gains in our ability to diagnose dementia with brain scans and cerebral spinal fluid analysis and some evidence from DNA assessment, memory loss is the most robust symptom of dementia. Personality changes, language impairment, and deficits in intellectual abilities and judgment, agitation, impulsivity, aggression, apathy and circadian rhythm disruption are also characteristic.

The most commonly diagnosed dementia is Alzheimer’s disease. Up to 75% of the cases of dementia will include Alzheimer’s disease. There is a range of differing diagnoses for kinds of dementia, but most are considered to be a type of spectrum disorder, one commonly associated with and sometimes promoting another. For example, strokes and vascular disorders may be precursors to a molecular cascade of cell changes that result in Alzheimer’s dementia.

There are different etiologies and symptoms depending on the kind of dementia that is in progress. We know that certain families may have a genetic loading for these disorders. We also know that high blood pressure, diabetes, toxic exposure, head trauma and other factors may play a significant role in their development. In Alzheimer’s disease symptoms worsen, while in vascular dementia they may be less predictable or even improve over time. Sudden onset dementias are potentially reversible and are usually related to metabolic, vascular, toxic or infectious disturbances.

Over 5 million Americans between the ages of 65 and 74 now have dementia. One of the reasons for this increase is that more people are living into old age. At 85 and older, a frightening 40% will be demented. The cost of care for Americans with dementia is over 150 billion dollars yearly. Nursing home care averages 7 to 12 thousand dollars monthly, not including medications. It is hard to imagine how we will be able to continue care for the demented of the baby boom generation and beyond.

We do not yet have drugs that can actually stop the downward progress of dementia. However, the medications that we do have may diminish the rate of decline, and several are now on the market. Other psychiatric medications are used to control emotional and behavioral symptoms, but recent data indicates an increase in mortality in demented elderly patients taking antipsychotic medications. As a result, it is recommended that they be used cautiously and for no longer than 3 months.

Are there life strategies that may help us to avoid dementia? While we do not know exactly how one may keep from contracting dementia, we do know that avoiding certain risk factors may help. These include diabetes, high blood pressure, high cholesterol and emotional stress. Depression and worry raise stress hormones that have long been know to damage brain cells in the short-term memory area. Depressed people have heightened white matter fiber connection between certain areas that are not seen in people who are not depressed. Does this mean that our lifestyle, experience and thinking patterns can rewire brain-signaling networks? You bet.

Exercise, good nutrition, healthy sleep habits and continued learning seem to nurture brain health. People who are highly educated, or who keep their minds active, seem to develop what are called, “cognitive reserves” which may help compensate for neuronal loss. This is because new synaptic connections are established between neurons in the brain when a person learns. With more knowledge our very plastic brains may increase connections and possibly adapt to dementia losses by finding alternative pathways. The learning process results in an increase in a brain chemical called Brain-Derived Neurotrophic Factor (BDNF). Because it seems to promote healthy brain cells, some neuroscientists think of this natural chemical as brain fertilizer.

In many ways research in dementia has transformed our understanding of the human brain and how it goes astray in this disease. We have new comprehension of the mechanisms of brain circuitry and its primary role in brain function. We have increased clarity of the spectrum relationship between differing kinds of dementia. While we have made progress in the area of diagnosis, treatment options remain limited. We have only been able to diminish the progress of dementia, not stop it.

- Dr. Linda Klaitz, Medical Psychologist


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