AgD (argyrophilic grain disease)

I ran across this short description of AgD recently on the Alzheimer Europe website. I’ve been sharing it with the folks I know whose family members are diagnosed upon brain autopsy with PSP *plus* AgD. It’s easier to post it here and send people to a link at this point.

CurePSP has copied most of the info on its website. I wish CurePSP had said more about PSP and how many PSP brains have AgD, according to Dr. Dickson.

—————————– … isease-AGD

Argyrophilic Grain Disease (AGD)
Neuro-Degenerative Diseases

by André Delacourte & Kurt Jellinger

General outline

New disease, which is not fully characterised. A sporadic late-onset form of dementia characterised by a neuro-degenerative process, which mainly affects limbic structures (amygdala, hippocampus and mediobasal temporal/entorhinal cortex).

It is named after silver-staining (argyrophilic) grains or coiled bodies within the cytoplasm of neurons that consist mainly of tau protein isoforms with four microtubule-binding repeates (4-R tau).


Braak’s disease

Symptoms and course

Reduction of short-term memory, disorders of word finding, disorders of reading and writing, disorientation, behavioural disturbances (personality changes, emotional disorders with aggression and ill-temper) may precede or follow memory failure. Clinically it is hard to distinguish from late-onset AD.

The age of onset is around 70 years old. The duration of the disease is between 4 and 8 years.

Causes and risk factors

Neuron degeneration likely associated with dysfunction of tau protein. Grains are composed of abnormally phosphorylated tau protein with 4 repeats. Recent studies indicate that tau protein dysfunction in AGD in contrast to other 4-R-tauopathies (progressive supranuclear palsy, corticobasal degeneration).


The disease arises irrespective of the genetic background regarding tau H1 or H2 haplotypes, at the opposite of PSP and CBD (Miserez A. R. et al, 2003). Lack of relationship with apolipoprotein E4.


1 to 5% of AD patients (Togo T. et al, 2002).

Diagnostic procedures

It is almost impossible to distinguish from late-onset Alzheimer’s disease. The diagnosis is almost entirely made by post-mortem examination. AGD lesions are found in about 5% of Alzheimer’s disease (Togo T. et al, 2002).

Care and treatment

Those related to patients affected by Alzheimer’s disease.

Ongoing research / clinical trials

Continued research on tau protein. Subclasses of AGD may exist, with a more diffuse forms of grain pathology (Maurage C. A. et al, 2003).

Last Updated: Friday 09 October 2009

“Deciding to Die, Then Shown the Door” (NYT)

This is quite a story in the New York Times about a couple deciding not to eat/drink any more, and then being forced to leave their care facility:

The New Old Age: Caring and Coping
Deciding to Die, Then Shown the Door
The New York Times
By Paula Span
August 24, 2011, 1:59 PM

In our local support group, we’ve had many people who have decided to stop eating and drinking.  I only know of one case where this decision was treated as a “problem.”  Recently, a woman who had progressive supranuclear palsy (PSP) for several years wanted to stop eating/drinking.  The woman was on hospice at this time.  Her daughter talked to the hospice agency about her mother’s wishes.  The hospice agency said that they could not discuss this topic with either the mother or the daughter.  So the daughter had to learn about dying in this manner on her own, and had to rely on others for support during this stressful time.  The mother did decide to stop eating/drinking.  This was communicated to hospice after several days.  At that point, the hospice agency returned to being supportive again (mostly).  The daughter kept in touch with me throughout this process (as we made brain donation arrangements), and reported that many friends and family were able to visit during this time.  The mother died peacefully.  Well before her death, she requested that her brain be donated.  (Mayo Jax confirmed the PSP diagnosis.)

The Multiple Phenotypes of CBS/CBD (Boeve article)

This review article by Dr. Brad Boeve of Mayo Rochester, one of the world’s experts in CBS/CBD, is a good one. It’s a short summary of our current knowledge about CBS and CBD.

Here are a few highlights:

* When thinking of CBS and CBD, “[there] are few other syndromes and diseases in the neurodegenerative disease field that are as complex and frustrating for patients, their relatives, the clinicians involved in their care, the pathologists who analyze tissue, and the scientists devoted to their study.”

* There are primarily six clinical syndromes that are associated with CBD pathology:

#1 behavioral variant frontotemporal dementia
#2 progressive apraxia of speech or progressive aphasia syndrome (PNFA is the most common though SD and LPA can occur) [PNFA = progressive nonfluent aphasia. SD = semantic dementia. LPA = logopenic progressive aphasia]
#3 corticobasal syndrome
#4 PSP Richardson syndrome [PSP = progressive supranuclear palsy]
#5 dementia syndrome highly consistent with probable Alzheimer’s Disease
#6 posterior cortical atrophy

There are “other rare variants” besides these six.

* The clinical syndrome CBS has many underlying diseases or pathologies associated with it — CBD, PSP, AD, Pick’s Disease, etc. “On one level, this heterogeneity is difficult to explain, yet a unifying pathologic feature of all of these diseases is the maximal involvement of the parietofrontal cortex and their afferent and efferent projections. The topographic distribution of neurodegeneration, therefore, dictates the clinical syndrome.”

I’ve copied the abstract below.


Here’s the abstract:

Journal of Molecular Neuroscience. 2011 Aug 19. [Epub ahead of print]

The Multiple Phenotypes of Corticobasal Syndrome and Corticobasal Degeneration: Implications for Further Study.

Boeve BF.
Divisions of Behavioral Neurology and Movement Disorders, Department of Neurology, Mayo Clinic, Rochester, MN, USA

Corticobasal degeneration (CBD) is a complex neurodegenerative disorder which nomenclature of which its nomenclature and characterization continues to evolve. The core clinical features that have been considered characteristic of the disorder include progressive asymmetric rigidity and apraxia, with other findings suggesting additional cortical (e.g., alien limb phenomena, cortical sensory loss, myoclonus, and mirror movements) and basal ganglionic (e.g., bradykinesia, dystonia, and tremor) dysfunctions.

The characteristic findings at autopsy are asymmetric cortical atrophy that is typically maximal in the frontoparietal regions, as well as basal ganglia and nigral degeneration.

Microscopically, abnormal accumulations of the microtubule-associated tau protein are found in both neurons and glia, and this disorder is now considered one of the “tauopathies.”

CBD was initially thought to represent a distinct clinicopathologic entity. Recent studies have shown considerable clinicopathologic heterogeneity, leading some to use the term “corticobasal syndrome” (CBS) for the constellation of findings initially considered characteristic of the disorder, and the term “corticobasal degeneration” for the histopathologic disorder.

In this review, the multiple phenotypes/syndromes associated with CBD pathology, and multiple diseases associated with the CBS, are presented. The clinicopathologic heterogeneity in CBS/CBD and the implications of this heterogeneity on clinical practice, on understanding the focal/asymmetric cerebral degeneration syndromes, and on future research are all reviewed.

PubMed ID#: 21853287 (see for this abstract only)

Overview of Lewy Body Dementia (2006, AlzOnline)

The University of Florida runs the “AlzOnline” program, online caregiver support for Alzheimer’s caregivers. From time to time, an article in their “Reading Room” catches my eye. Tonight, I ran across their 2006 overview of Lewy Body Dementia. This section is particularly good — “Family Education and Planning Ahead After the Diagnosis.” I’ve copied most of the text below but I think it’s a lot easier to read on the AlzOnline website.


Lewy Body Dementia
AlzOnline (University of Florida)

According to some researchers, Lewy body dementia (also called Lewy body disease or dementia with Lewy bodies) now ties with vascular dementia as the second most commonly occurring progressive dementia after Alzheimer’s disease, the most common progressive dementia.1, 2, 3

[Note: Dementia, a decline in thinking and/or memory function while the person is awake and alert, interferes with normal daily functioning. Progressive dementia becomes worse over time.]

Early symptoms of Lewy body dementia (LBD) typically include a mixture of difficulties with fluctuating (changing) attention, alertness and cognitive (thinking and memory) skills, personality changes and movement (motor) difficulties.3, 4 There does not appear to be a strong tendency for inheriting the disease; few reports describe families with the autosomal dominant version of LBD.5

Lewy Bodies in the Brain
The name for the protein deposits called Lewy bodies comes from Friedrich Lewy (1885 – 1950) who studied under Dr. Alois Alzheimer in 1912 and who identified the special spheres in the cells of brainstem tissue.6 Since then, Lewy bodies have been identified elsewhere in the brain, especially in the cortex and limbic system. In 1961 research linked Lewy bodies to progressive dementia.7

The Lewy bodies seem to concentrate in the neocortex, the top part of the brain primarily responsible for cognitive or thinking and memory functions; the limbic cortex primarily responsible for emotion and behavior), the subcortical nuclei (primarily responsible for motor functions), and the brain stem (also primarily responsible for motor functions). Some researchers think that the unstable (on/off) activity in LBD relates to decline in the brain cell connections (ascending cholinergic projections) from the brainstem that project forward to brain cells that control attention.8, 9

Lewy Body Dementia (LBD) versus Alzheimer’s Disease versus Parkinson Disease
Guidelines for diagnosing Lewy body dementia (LBD) come from a 1996 consensus conference of experts with updates published in 2005.3, 10 The classical signs of LBD include changes (unexplained fluctuations) in thinking and memory functions, vivid visual hallucinations and parkinsonism.3, 10, 11

The changes of LBD differ from those of Alzheimer disease and Parkinson disease. In LBD early changes involve fluctuating attention and alertness (episodes of “tuning out” sometimes like a light switch turning off and then on again), visual hallucinations and slowness and stiffness in movement. Persistent difficulties with short-term memory and recalling specific names of people or objects show up much later in LBD.

In Alzheimer disease, early difficulties usually involve short-term memory and recalling specific names of people, places or objects words while much later there are problems with movement and sometimes hallucinations.

The classic early features of Parkinson disease are 1) tremor in the arms or legs (sometimes the head) when the limbs (or body) are at rest but which fade when the limbs move purposefully (to do a task), 2) slow movement, stiff movements, and 3) problems walking. Often depression occurs and may begin before the movement difficulties show up. Many people, but not all, with Parkinson disease experience slow decline in thinking and memory functions during the course of the disease. A brief trial of a dose of sinemet (medicine) which shows improvement in tremors and movement confirms a diagnosis of Parkinson disease. Some people with Parkinson disease develop only difficulties with movement and never develop decline in thinking and memory functions.

Changes in Attention
An early typical sign of LBD is occasional loss of attention and alertness, the “on-off” sign when thinking and memory abilities fade out and the person phases out from conversations or activities. Moments of clear function may switch to states of confusion that may affect conversation and activities such a preparing a meal, personal care, or walking. These problems may be worse for a couple of hours and then the person may return to normal functioning or the problems may last a few hours or days. This behavior is not delirium, which is a rapid change in thinking and actions often caused by infection, over-medication, dehydration or other usually treatable temporary health problem; when medically treated, delirium disappears. Family members have described the LBD-related changes in attention and alertness as the person’s mind being “some place else” and the person’s face getting a “glazed look”. Others have described it as being “unconscious, but awake”.

Thinking and Memory Difficulties (Cognitive and Memory Decline)
Early on in LBD short-term memory problems may be very mild while there may be more difficulty with maintaining attention, staying focused, making good decisions and completing a task.

Later, as the LBD progresses the person may begin struggling with directions to a new place or may get lost while driving in familiar places. They may have more difficulty responding appropriately during a conversation, such as finding the right words to express themselves or staying on the topic. Ultimately, the memory, language and other thinking abilities worsen. Eventually, the caregiver serves as the memory, decision-maker, communicator, etc. for the person with LBD.

Hallucinations usually involve images (seeing people, animals, objects or designs that are not present) but may be auditory (hearing voices or sounds that are not present). Early in the course of the LBD the person typically has visual (sometimes auditory) hallucinations or (rarely) both. Often the person is aware that the visual image, though vivid, is not real. Usually these images are pleasant, representing people and pets that provide pleasant feelings and distractions.

Hallucinations tend to upset the family more than the person seeing the images. If the person who hallucinates is not upset, the family should accept the situation. Hallucinations are treated when they frighten the person or lead to unsafe behaviors. Sometimes people with hallucinations also have delusions (false ideas about a person, animal or situation). The delusions may involve suspicions of harm such as someone intending to rob or attack them.

When the hallucination is unpleasant or frightening, steps should be taken to change the setting (such as covering mirrors, increasing light to a room or removing furniture that looks like a frightening animal). It may help to comfort the person by pointing out the real identity of the image or noise; it may be more comforting to provide a pleasant distraction such as music, going to a different room or outside, changing the activity such as going for a car ride or walk, or taking a break for a snack or drink of water.

Movement Difficulties (Motor Decline)
Movement difficulties may show up as stiffness in moving the neck or spine, which physicians call mid-line rigidity. Stiffness and slowness in the muscles of the arms may result in slow arm or leg movements. There may be less facial expression. Some people will report new problems with walking, shuffling steps with walking or tripping when using the stairs. They may have problems getting into and out of a car. These movement difficulties fall into the group of parkinsonism features; parkinsonism features are not the same as Parkinson disease though there may be an overlap in nerve cells and nerve paths that are affected. A brief trial of sinemet (medicine) may help significantly and thus indicate that the condition is Parkinson disease. Sometimes in the case of LBD, sinemet or a similar medicine may help to improve body movement; however, the sinemet may offer no help, may increase hallucinations and may interfere with sleep.

The person may develop clumsiness when doing tasks using skilled hand movements. When the repair person of the family no longer can fix the plumbing or the family cook no longer can use the kitchen tools, the brain control of learned skilled movements may be in decline. Decline of skilled movement is called apraxia. As LBD continues, skilled movements and general body movements become more difficult and may lead to immobility and the need for help with all tasks or total care.

Sleep Disorder
The REM (rapid eye movement) stage of sleep is an early phase of sleep. A REM sleep disorder may be an early sign of LBD. Sometimes people with a REM sleep disorder move in ways that actively reflect what they are dreaming. Their movements may reflect vivid frightening dreams, thus they kick their legs, swing out their arms and speak or yell out during this stage of sleep. For some reason the brain has not released the controls to the signals that stop muscle movement during dreaming and thus movements occur during this stage of sleep. Essentially, they are asleep, unaware of this activity while acting out their dreams.11, 12

Early in the course of LBD or much later there may be signs of depression, such as increased irritability, poor concentration, lack of attention during interactions, sadness or a negative mood, poor appetite or sleep, or the opposite over-eating and sleeping too much (14 or more hours of sleep over a 24 hour period is too much sleep). Withdrawal from normal activities is another sign of depression. The depression should be treated for as long as the depression lasts.

SSRI (selective serotinergic reuptake inhibitors) are preferred in most cases as the medicine of choice when prescribing an antidepressant for someone with a progressive dementia.

NOTE of CAUTION regarding neuroleptics or antipsychotic drugs: Neuroleptics or antipsychotic drugs may be prescribed to treat difficult-to-manage behaviors and hallucinations and may result in extreme behaviors opposite to the expected calming behavior. Adverse reactions may result and may not stop even after the medicine has been stopped.10, 13-16

Medical Evaluation
The medical evaluation should include a physical exam, a neurological exam, information about the person’s medical and surgical history, family (medical) history, social history, a list of prescribed and over-the-counter medicines as well as vitamins, minerals, herbs, etc. Blood tests should evaluate electrolytes, sedimentation rates, cholesterol, triglycerides, urea, liver functions, vitamins such as folate and B12, body hormones such as thyroid, and infections. Also important are a brain image (CT or MRI) and evaluation of the heart and blood circulation systems. An EEG (electro-encephalogram) may help to rule out seizures. A spinal tap helps to rule out infection or other reasons such as normal pressure hydrocephalus for the progressive dementia. According to some researchers, past experiences of low tolerance to neuroleptic medicines may indicate a risk for LBD.1, 3, 10

The brain cell changes from LBD result in less dopamine and acetylcholine, two message-carrying chemicals important to efficient brain function. In addition, to living a healthy lifestyle (regular physical exercise, social activities, brain exercise, and good nutrition), three anticholinesterase medicines are available to optimize memory and thinking functions: donepezil (aricept), rivastigmine (exelon), and galantamine (razadyne, previously known as reminyl).10, 17, 18 The anticholinesterase medicines seem to decrease the frequency and intensity of hallucinations, decrease agitation and improve cognitive function. Memantine (namenda), medicine also prescribed for people with a diagnosis of progressive dementia1, is still undergoing research regarding its usefulness in LBD.

It is important to avoid any medicines (prescribed or over-the-counter) or other supplements that have an anticholinergic effect (a chemical effect that interferes with or lessens memory and thinking functions and may increase sleepiness and risks for imbalance or falling). Good sources to learn about anticholinergic effects of medicines, etc. are a physician and a pharmacist (ask both people!).

Difficulty getting to sleep or maintaining a healthy amount of sleep for good rest and body restoration should be evaluated. There may be a medical explanation and treatment for the sleep problem. Often improving sleep hygiene, such as a quiet setting for sleep, decreasing foods or drinks with caffeine, fat and refined sugars several hours before bedtime, and good exercise during the day, increase sleep hunger (feeling a need to sleep). It is important also to schedule quiet, calming activities before bedtime; thus, no arguments, no balancing bank statements, no murder mysteries, and no sensational T.V. news stories before bedtime. Instead one may try a warm foot soak, a glass of warm milk (an old-fashioned remedy that recently has regained respect), listening to soothing music, softer lighting, looking at pleasant family photographs to stir up pleasant memories, self-massage on the arms and legs with a pleasant-smelling lotion, reading a boring book.

After the Diagnosis
Family Education and Planning Ahead After the Diagnosis
After the medical evaluation and the diagnosis, education about the condition and planning ahead are essential for long-term care management.19 Education will help one understand the areas of good function, the areas of difficulty, and the changes to expect over time, though the type and rate of changes differ from person to person.

Education may help the family caregivers anticipate changes in behavior or capability and modify the home setting to make self-care easy as the person experiences progressive decline. Evaluations of the home setting should focus on modifying the setting rather than trying to modify the person with the diagnosis. The approach of modifying the setting may decrease caregiver stress and patient frustration.19, 20

As soon as possible family matters, such as financial, legal, and health planning, should be discussed and organized. These plans should be discussed with at least one trustworthy person who does not live under the same roof as the person with LBD. A storm or other disaster that creates electrical shortages or destroys the home may lead to a temporary move to another setting. If the people at this temporary setting have information about the daily care needs of the person with LBD, it should smooth the transition and the adjustment to the temporary setting. Back-up plans should consider resource people, such as family or neighbors, and resource programs and services such as local support groups and chapters of the national Alzheimer’s Association or Alzheimer Resource Centers. A Checklist on Family Matters is available to guide planning ahead.19

Planning ahead tasks should consider issues of safety, exercise (physical, emotional, social, and spiritual) as well as brain exercise, mobility, nutrition, physical health, dental health, personal interests such as hobbies and preferences (for example, in activities and diet), and end-of-life choices.19

Resources to help caregivers should be identified and accessed whenever appropriate. Resource programs include local chapters of the Alzheimer’s Association, other groups who deal with progressive dementia such as the Alzheimer Resource Centers, adult day (health) care programs, senior centers, meal sites, religious organizations with programs or special services, assisted living facilities, nursing homes, alternative transportation when the family unit no longer has an available driver, volunteer groups and neighbors. Helpers include not only health and social service providers but also care managers who help address the daily needs of the family and the household.20

The family may choose to plan ahead regarding physical and occupational therapy evaluations of the person and the home to install helps such as a hand rail in hallways and features in the kitchen and bathroom to assure safety with changes in mobility. For example, safety tips may include increased lighting in darker corners of the house and cutting down on sunlight glare in extremely bright rooms when the sun rises or sets. Suggestions for people who have a problem with balance or light-headedness may include sitting on a chair while exercising, bathing in a shower, or while brushing ones teeth.

Exercise Suggestions:
The physician, physical therapist, and occupational therapist may offer suggestions and routines for daily exercise such as the following:

Walking; short walks with occasional rest stops on a bench or chair
Pet care: brushing the dog or cat
Watering indoor or outdoor plants; yard work; blowing bubbles outdoors
Washing the car
Winding yarn or thick thread around a spool, paper tube or old tennis ball
Chair exercise:
a. while seated in a sturdy chair (with side support), lift arms and legs, in a series of moves
b. march in place (feet on the floor while seated)
c. kick the ball; volley ball with a balloon
For people who move slowly: after asking a question or when starting an activity, allow 15 seconds or more (count silently to 15 or 20) to allow the person enough time to respond.

Family and paid caregivers must have respite (take regular timeout for “down time”, rest and relaxation). Family caregivers, especially, get help before actually needing it to avoid burnout or a physical collapse. If the caregiver is wondering, “Is it time to get help?”, then it is time! Getting help when a person is on the point of physical or emotional collapse may be too late to keep the caregiver, the family unit, the extended family and household functioning well.

1. Barber, R., Newby, J., & McKeith, I.G. (2004). Lewy body disease. In Ralph W. Richter & Brigette Zoeller Richter (Eds.). Alzheimer’s Disease. Totowa, N.J.: Human Press, 127-135.

2. Hansen, L., Salmon, D., Galasko, D., Masliah, E., Katzman, R., DeTeresa, R., Thal, L., Pay, M.M., Hofstetter, R., Klauber, M., et al. (1990). The Lewy body variant of Alzheimer’s disease: A clinical and pathologic entity. Neurology, 40(1),1–8.

3. McKeith, I.G., Galasko, D., Kosaka, K., Perry, E.K., Dickson, D.W., Hansen, L.A., Salmon, D.P., Lowe, J., Mirra, S.S., Byrne, E.J., Lennox, G., Quinn, N.P., Edwardson, J.A., Ince, P.G., Bergeron, C., Burns, A., Miller, B.L., Lovestone, S., Collerton, D., Jansen, E.N., Ballard, C., de Vos, R.A., Wilcock, G.K., Jellinger, K.A., Perry, R.H. (1996). Consensus guidelines for the clinical and pathologic diagnosis of dementia with Lewy bodies (DLB): Report of the Consortium on DLB International Workshop. Neurology, 47(5),1113–1124

4. Perry, R., McKeith, I. & Perry, E. (Eds.). (1996). Dementia with Lewy Bodies: Clinical, Pathological and Treatment Issues. NY: Cambridge University Press.

5. Wakabayashi, K., Hayashi, S., Ishikawa, A., Hayashi, T., Okuizumi, A., Tanaka, H. et al. (1998). Autosomal dominant diffuse Lewy body disease. Acta Neuropathology, 96, 207-210.

6. Lewy, F.H. (1912). Paralysis agitans. In Handbuch der Neurologie (Edited by: Lewandowsky M). Berlin: Springer Verlag, 920-933.

7. Okasaki, H., Lipkin, L.E., & Aronson, S.M. (1961). Diffuse intracytoplasmic inclusions (Lewy type) associated with progressive dementia and quadriparesis in flexion. Journal Neuropathology and Experimental Neurology, 20, 237-244.

8. Perry, E.K., & Perry, R.H. (1996). Altered consciousness and transmitter signaling in Lewy body dementia. In Perry, R., McKeith, I.G., & Perry, E. (Eds.). Dementia with Lewy Bodies: Clinical, Pathological and Treatment Issues. NY: Cambridge University Press, 397-413.

9. Dickson, D.W. (2001). Neuropathology of Alzheimer’s disease and other dementias. Clinical Geriatric Medicine, 17(2), 209-28.

10. McKeith, I.G., Dickson, D.W., Lowe, J., Emre, M., O’Brien, J.T., Feldman, H., Cummings, J., Duda, J.E., Lippa, C., Perry, E.K., Aarsland, D., Arai, H., Ballard, C.G., Boeve, B., et al. (2005). Diagnosis and management of dementia with Lewy bodies: Third report of the DLB Consortium. Neurology, 65(12),1863-1872.

11. Knopman, D.S. & Jankowiak, J. (2005). Not all dementia is Alzheimer: Dementia with Lewy bodies. Neurology, 65, E26-E27.

12. Boeve, B.F., Silber, M.H., & Ferman, T.J. (1999). Association of REM sleep behavior disorder and neurodegenerative disease. Sleep, 22; S72.

13. Bymaster, F.P., Calligaro, D.O., Falcone, J.F., et al. (1996). Radioreceptor binding profile of the atypical antipsychotic olanzapine. Neuropsychopharmacology,14, 87-96.

14. Burke, W.J., Pfeiffer, R.F., & McComb, R.D. (1998). Neuroleptic sensitivity to clozapine in dementia with Lewy bodies. Journal of Neuropsychiatry and Clinical Neurosciences, 10, 227-229.

15. McKeith, I., Fairbairn, A., Perry, R., Thompson, P., & Perry, E. (1992). Neuroleptic sensitivity in patients with senile dementia of Lewy body type. British Medical Journal, 305(6855):673-678.

16. Miller, C.H., Mohr, F., Umbricht, D., Woerner, M., Fleischhacker, W.W., & Lieberman, J.A. (1998). The prevalence of acute extrapyramidal signs and symptoms in patients treated with clozapine, risperidone and conventional antipsychotics. Journal of Clinical Psychiatry, 59, 69-75.

17. Kaufer, D.I., Catt, K.E., Lopez, O.L., & De Koskey, S.T. (1998). Dementia with Lewy bodies: Response of delirium-like features to donepezil. Neurology, 51, 1512.

18. Perry, E.K., Marshall, E., Thompson, P., et al. (1993). Monoaminergic activities in Lewy body dementia: Relation to hallucinosis and extrapyramidal features. Journal of Neural Transmission 6, 167-177.

19. Doty, L., Heilman, K.M., Stewart, J.T., Bowers, D., & Rothi, L.G. (1993). Case management in Alzheimer’s disease. Journal of Case Management, 2(4),130-136.

20. Zarit, S.H., Stephens, M.A., Townsend, A., & Greene, R. (1998). Stress reduction for the family caregivers: Effects of adult day care use. Journals of Gerontology Series B: Psychological Sciences and Social Sciences, 53(5), S267-S277.

Prepared by: Leilani Doty, PhD, Administrator, Florida Department of Elder Affairs, Alzheimer’s Disease Initiative, University of Florida Memory Disorder Clinic (MDC),Box 100236, McKnight Brain Institute, Gainesville, FL 32610-0236, Office (352)273-5555; MDC Appointments: (352)265-8408 (2006)

Helping protect your aging parent from financial pitfalls

Local support group member Ellen shared this Morningstar article with me at Sunday’s caregiver support group meeting.  The article doesn’t contain investment advice, but rather contains info on “key actions to consider that can help protect you or an aging parent from the financial pitfalls associated with cognitive decline.”

The sections on “Documenting Decline” and “A Sensitive — and Critical — Issue” discuss the issue of cognitive decline and poor financial decision-making.

After digging around, I found parts of the article on two different websites:

The Smart Investor
Eight steps to wealth protection for aging investors
By Mark Miller

Happy reading,