The New York Times has a very nice article about Frontotemporal demetia (FTD). This type of dementia is interesting, affecting personality, inhibition, attention, and language. It is similar to Alzheimer’s Disease but has a different progression and manifestation. Anyway, the article provides a nice picture of the disease.
Parkinson’s disease (PD) affects an estimated 1.5 million Americans and about 2% of people over 65 in the U.K. Its prevalence increases with age, although roughly 15% of Americans with Parkinson’s disease are 50 or younger. Parkinson’s disease is part of a broader spectrum of disorders known as parkinsonism. While it was viewed as fairly homogeneous in the past, researchers and clinicians now recognize the complexity of the disease and its related diseases.
The defining neurological marker of Parkinson’s disease is the destruction of the substantia nigra pars compacta, a small nucleus in the brain that is one of the major dopamine-producing brain areas. Symptoms of PD are not evident until around 80% of the neurons in the substantia nigra (literally translated as “black substance”) are destroyed. Because the substantia nigra produces dopamine, which is an important neurotransmitter, the depletion of dopamine in the brain that is associated with PD affects the striatum, which in part suppresses the subthalamic nucleus. This in turn results in more activity in the globus pallidus and substantia nigra pars reticulata, which in the end leads to more activation of the inhibitory thalamic nuclei that are involved in motor functioning. To summarize, decreased dopamine results in decreased motor activation as well as other motor problems.
The common features of Parkinson’s disease are easily remembered by the mnemonic TRAP.
- T – Tremor, specifically resting tremor. Tremor that occurs when moving (e.g., reaching for an object) is called essential tremor and is not a defining characteristic of PD; in fact, it is a different but related disorder.
- R – Rigidity. Difficulty moving and stiff arms and limbs.
- A – Akinesia. No or slow movements.
- P – Postural instability. Posture problems.
Gait abnormalities is also one of the common features of PD. It is especially useful for detecting the disease early in the process. The common gait problems are decrease height and length of step and less arm swing (i.e., walking more with a shuffle than a normal gait). People with PD also often take very small steps when turning around.
PD patients often have difficulty swallowing saliva so they often drool. They also often have micrography (very small writing) that progressively gets smaller with prolonged writing. Depression is common in PD patients as well. If given levodopa (L-dopa) they will respond. Symptoms of dementia often occur as well but they usually occur after a few years post diagnosis. However, there are often more mild cognitive changes early on in the disease process, such as slowed processing speed and slowed reaction time.
Reference
Approach to diagnosis of Parkinson disease (C. Frank, G. Pari, & J. P. Rossiter, 2006). Canadian Family Physician, 52, 862-868.
I’ll start with the bad news first. The human brain reaches it’s physical peak around the age of 25. After that it’s all downhill. The prefrontal cortex and underlying white matter is the last area of the brain to develop (including myelination); that area is also the first to start the decline. Myelination of the frontal cortex typically isn’t completed until the early to mid 20s. Its slow degradation starts quickly after it finishes development. This slow degradation of the brain correlates with slowed processing speed initially and, later in life, with declines in all areas of cognition. The good news is that cognitive performance in most areas does not typically decline until the mid 50s; many abilities such as verbal continue to increase until the mid 50s or early 60s. While there is often global brain matter loss (slowly over the decades), specific areas of the brain change at different rates (with some areas exhibiting volume increases until the mid 50s or so).
This news can be discouraging for people who are older than 25 (such as myself) – knowing that I am on the downward slope, at least as far as brain volume, myelination, and processing speed are concerned. I wrote about the bad news first so now the good news. Even though cognitive performance starts to decline, on average, in the mid 50s, many domains increase between age 25 and age 55; thus, the declines in late life often merely bring cognitive performance back down to where it was in the mid 20s. Of course processing speed in late life is a lot lower than in the early 20s but verbal memory and abilities, reasoning, and spatial abilities are quite intact in late life. Math abilities tend to decrease significantly over life though. The graph shows cognitive performance as measured by a 35-year longitudinal study (actually a sequential research design – both cross-sectional and longitudinal) (Schaie, K. W. Intellectual Development in Adulthood: The Seattle Longitudinal Study. Cambridge Univ. Press, Cambridge, 1996).
For a comprehensive review of cognitive and neurological changes associated with aging read Trey Hedden and John D. E. Gabrieli’s Nature Review: Neuroscience article published in February 2004. I’ve included a link to a PDF of the article: Aging article.
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.
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.
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.
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