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Natural Human Antibodies for Alzheimer Disease

Natural Human Antibodies for Alzheimer Disease

Teaser: 

Click here to view the entire report from the 4th Canadian Colloquium on Dementia

The Alzheimer’s Disease Symposium: Immunotherapies, the Question of Cures, and the Amyloid Hypothesis

Moderator: John R. Wherrett, MD, FRCP(C), PhD, Professor Emeritus, Division of Neurology, University of Toronto; consultant in Neurology, Toronto Western Hospital and Toronto Rehabilitation Institute; member, Memory Clinic, Toronto Western Hospital, Toronto, ON.
A panel of four high-profile researchers discussed current horizons of research in Alzheimer’s disease and related dementias.

Natural Human Antibodies for Alzheimer’s Disease

Speaker: Dr. Norman Relkin, MD, PhD, Director, Cornell Memory Disorders Program, New York Presbyterian Hospital; Weill Cornell Medical College, New York.
Neurologist Dr. Norman Relkin detailed his and others’ work in the field of immunotherapy for Alzheimer’s disease (AD).

Noting that disease treatments tend to reflect prevailing pathological hypotheses, Dr. Relkin observed that current drug therapies for AD reflect the so-called cholinergic hypothesis of the previous few decades. Today, most studies focus on the role of beta-amyloid, and there are presently more than 30 trials underway that pursue the amyloid hypothesis. These research approaches encompass the transcription and translation of the APP gene, the production of amyloid monomer, the aggregation process, the formation of diffuse plaques in the brain, and the inflammatory processes that convert the formation of plaques in the brain associated with AD.

Dr. Relkin reminded listeners that immunotherapy is a class of treatments, not a single therapy. Immunotherapies include any approach that harnesses the actions of the humoral (B-cell mediated) and/or cellular (T-cell mediated) immune system. Immunotherapy initially came to the fore after Dr. Dale Schenk and colleagues found that an amyloid “vaccine” reduced the burden of plaques and memory loss in a transgenic mouse model of AD. The effect was demonstrated in the case of established plaques as well, despite the former thought that plaques were immutable.

The first use of antiamyloid immunotherapy in humans with AD showed similar clearing of amyloid plaques. However, due to a harmful T-cell mediated response, an unacceptably high number of patients developed meningoencephalitis. Subsequently, researchers sought to define and preserve the benefits of vaccination and eliminate the harmful response.

Dr. Relkin then described a developing approach called passive immunization, which involves supplying antibodies from an exogenous source, i.e., synthetic or animal. Dr. Relkin also drew attention to immunomodulation, a strategy that does not use the immune system directly but instead its chemical messengers, such as cytokines. All of the forms of immunotherapy he described are being pursued in current research.

Intravenous Immunoglobulin
Dr. Relkin further described a slightly different model of immunotherapy emergent over the last 4 years: intravenous immunoglobulin (IVIg), described in Figure 1.

Motivated by the safety concerns of amyloid immunotherapy, IVIg holds promise as something time-tested. IVIg is a pooled human Immunoglobulin G (IgG) preparation obtained by cold ethanol extraction from the plasma of thousands of healthy blood donors. It is already in use as a treatment for a number of immune deficiency disorders and other syndromes. IVIg contains natural antibodies, including antiamyloid antibodies.

Research data suggest that AD patients have fewer antiamyloid antibodies than nondemented individuals, making IVIg potentially valuable for such patients. IVIg has an established safety profile and is less likely than other immunotherapies to cause untoward events.

Dr. Relkin further detailed positive findings from his own research and that of Dr. Richard Dodel in Germany. Both studies’ Phase I data reflected a symptomatic benefit generated of IVIg over a 6-month period (these were add-on studies for patients under treatment with other agents), lowering the levels of amyloid in the blood. In the Relkin et al. study, a single IVIg low dose was followed by three higher doses. Each time the levels of antiamyloid antibodies were raised, there was a comparable impulse function in plasma amyloid curves. Dr. Relkin also presented data from his 18-month extended study. Significant results included marked decreases of the level of Ab40 and Ab42 in spinal fluid. Dr. Relkin then added a Mini-Mental State Exam measure to the study for safety purposes. He noted that the most robust response was seen among patients receiving the lowest doses of IVIg; a high number of low dose treatments also yielded positive results, in contrary to higher doses IVIg. Results were beyond expectations, the key finding being a disease stabilization effect over 18 months, Dr. Relkin stated. Given the positive interim results, they have announced they will be going to Phase III early in 2008.

Dr. Relkin noted some “paradoxes” in these data. Why do we have antibodies in our blood against Ab? Amyloid is a physiologic peptide we all produce from birth, for which the immune system should show tolerance. Researchers experimented with adding IVIg to Ab solutions in vitro: no binding response was exhibited. The response is mediated in the body by the effect of aggregation: amyloid can form soluble aggregates called oligomers, which are the targets of an antibody response. There is a peak of response corresponding to mid-sized oligomers, which means that the antibodies in IVIg are ignoring monomeric (benign) molecules and instead focusing on and binding to what Dr. Relkin described as very toxic species of reactive Ab. The “bottom line,” Dr. Relkin stated, is that the body is not indiscriminately fighting amyloid-it recognizes its toxic and misfolded forms.

The promise of this research, Dr. Relkin stated, is that oligomers are suspected to be the causative factors of a number of neurodegenerative diseases (AD, dementia in Down Syndrome, Lewy body dementia, Parkinson’s disease, Huntington’s, and others). These proteins circulate normally, but the oligomers represent pathological forms. This research suggests that there is an innate biological defense against neurodegenerative diseases, and IVIg holds promise as a tool to aid the fight (Table 1).

Alzheimer’s Disease: Treatments on the Horizon

Alzheimer’s Disease: Treatments on the Horizon

Teaser: 

Click here to view the entire report from the 4th Canadian Colloquium on Dementia

Alzheimer’s Disease: Treatments on the Horizon

Speaker: Dr. Serge Gauthier, MD, FRCPC, Director, Alzheimer Disease and Related Disorders Research Unit, McGill Centre for Studies in Aging, Montreal, QC.

Dr. Serge Gauthier focused his overview of current and future dementia treatments on the continuum of cognitive decline. He started with a “natural history of cognitive decline,” tracing cognitive deterioration’s trajectory from the earliest stages through profound impairment and death. The resulting picture is of a spectrum of cognitive abilities embracing the full range of health and pathology.

With this continuum in mind, Dr. Gauthier termed normal cognitive abilities as “pre-Mild Cognitive Impairment.” Such individuals might have subjective memory complaints, but these are undemonstrated in testing.

The next position on the spectrum was “Amnestic MCI” or “Predementia Alzheimer’s Disease.” This may be a prodromal phenomenon, Dr. Gauthier explained. These individuals he called “the forgetfuls,” noting that some but not all have pre-dementia Alzheimer’s disease (AD). Current symptomatic treatments for this stage include antidepressants and cholinesterase inhibitors (ChEI).
The choice of medication and the development of future treatments is connected to the concept of disease progression (Figure 1). He advised the audience to recall the difference between disease-modifying versus symptomatic drugs. With the latter, no improvement in the patient’s condition is expected, the criterion being only stabilization.

Dr. Gauthier cited a study by Winblad et al. from Neurology (2001) as evidence of donepezil’s benefit.1 He emphasized that this is a class effect: clinicians can expect improvement over baseline for 9-12 months for mild to moderate levels of impairment. Individuals with moderate to severe impairment living at home can expect improvement for about 6 months. In terms of cognition, patients will improve for anywhere from 6-12 months, depending on the severity of their cognitive decline.

Dr. Gauthier addressed the issue of combining agents, namely, memantine and donepezil in patients with mild dementia. He noted that studies have found additional improvement in cognition scores with the combined treatment over a period of 6 months.

In terms of agents on the horizon, Dr. Gauthier discussed the coming rivastigmine transdermal patch. The theoretical benefits, he stated, are clear. Recent studies confirm demonstrated benefit over baseline in MMSE scores. Similar benefits were demonstrated on the ADCS-ADL. The benefit with the patch is that higher doses may be achievable, without compromise to safety and tolerability.

Dr. Gauthier emphasized the value of Goal Attainment Scaling, as discussed by Dr. Kenneth Rockwood in the Canadian Medical Association Journal. Individual goal setting, in combination with galantamine, can be of value to patient care when real improvement in disease expression and progression is not expected, he noted.

The key idea, Dr. Gauthier stressed, is that symptomatic treatments for mild to severe stages of AD and related dementias are already available.

Modifying Disease among Mild AD Patients
Dr. Gauthier discussed disease modification among the patient group on the mild end of the spectrum of AD expression. In presenting details of two studies, he mentioned the caveat that the traditional study duration is sometimes inadequate to chart improvement among this treatment group. Eighteen months may be insufficient with mild AD patients.

Tramiprosate & Taranflurbil

Dr. Gauthier discussed treatment trials of the agent tramiprosate (Alzhemed®), an agent that binds to the soluble amyloid Ab. Phase III data from the clinical trial did not demonstrate statistical significance in favour of tramiprosate, with respect to the primary endpoints over 18 months of treatment. An advisory board of experts is currently reviewing data to see if benefit could have been measured differently. A European Phase III clinical trial is ongoing and could be modified based on North American findings.

The second agent Dr. Gauthier considered was taranflurbil (Flurizan®), a modulator of gamma secretase, currently in Phase II testing under lead investigator Dr. Sandra Black. The Phase II effort is to determine the most appropriate dosage. Patients in the study’s Canadian arm continued on the regime for an extra year. Key results showed that patients with mild AD who received a high dose of the medication obtained MMSE results indicating stabilization. Another surprise from the Phase II data was the statistically significant reduction of the psychiatric side effects. The protocol is ongoing for Phase III, and results are expected in December 2008.

Dr. Gauthier observed that there is room for improvement in the responder analysis: he offered that the 18-month baseline is not as useful a measure as it could be, and that a responder analysis would be useful. Further, delay to events-that is, the delayed emergence of significant psychiatric symptoms-would be a more meaningful measure of benefit, according to Dr. Gauthier. Disease-modifying drugs are under testing in mild AD, the primary hypothesis being that amyloid deposition is a major cause of the disease. The question remains, is this stage of dementia the best one for such pharmacotherapies?

A Closer Look at Mild Cognitive Impairment
Mild cognitive impairment (MCI), Dr. Gauthier emphasized, is neither a diagnosis nor a disease, but a way of defining cognitive deficit that has clinical utility. There will never be a drug for MCI, he stated. He presented results of a joint Canada-U.S. study comparing Vitamin E, donepezil, and placebo.2 The study found no difference in conversion rates at 3 years for any of the groups. At present, there is nothing to be given for MCI.

However, the data are different for predementia Alzheimer’s. Dr. Gauthier mentioned his recent position paper considering research criteria for the diagnosis of AD, published in 2007 in Lancet Neurology and advocating a change in the core diagnostic criteria.3

The ultimate effect of the changed criteria is to extend the determination of Alzheimer’s in a predementia stage. A diagnosis of the predementia stage of AD would become a clinical possibility and would be considered amenable to experimental treatments, with progression to dementia as a primary endpoint.

Conclusion: Controllable Risk Factors for Cognitive Decline
Dr. Gauthier predicted that control of risk factors will be integrated as part of the general stage-specific intervention schema. He noted specifically that education, dietary, and lifestyle factors have been correlated with cognitive effects. Incorporating measures to improve these factors will be integral to efforts to slow the conversion rate of pre-AD memory to dementia, and strategies to target them (such as interventions to control vascular risk factors) will be of key interest to researchers in coming years. This is fuelling study of agents such as ginkgo biloba. Dr. Gauthier advised predicted growing interest in the “triple approach” of diet (particularly the Mediterranean diet, shown to reduce risk by ~40%), exercise, and cognitive training. Overall, the focus of research and study for the next 5 years will likely reflect a preventive approach to cognitive impairment and the dementing syndromes.

References

  1. Winblad B, Engedahl K, Soininen H, et al. A 1-year, randomized, placebo-controlled study of donepezil in patients with mild to moderate AD. Neurology 2001;57:489-95.
  2. Peterson RC, Thomas RG, Grundman M, et al. Vitamin E and donepezil for the treatment of mild cognitive impairment. N Engl J Med 2005;352:2379-88.
  3. Dubois M, Feldman HH, Jacova C, et al. Research criteria for the diagnosis of Alzheimer’s disease: revising the NINCDS-ADRDA criteria. Lancet Neurol 2007;6:734-46.

Working Effectively with Community Partners in Dementia Care

Working Effectively with Community Partners in Dementia Care

Teaser: 

Click here to view the entire report from the 4th Canadian Colloquium on Dementia

Working Effectively with Community Partners in Dementia Care

Speaker: Dr. Carole A. Cohen, MD, FRCPC, Associate Professor, Department of Psychiatry, University of Toronto; Clinical Director, Community Psychiatric Services for the Elderly, Sunnybrook and Women’s College Health Sciences Centre; Toronto, ON.

Dr. Carole Cohen, a geriatric psychiatrist and academic, explored the wider “systems issues” associated with providing care to individuals diagnosed with dementia. These individuals’ care needs cannot be met solely within primary care. The key question, according to Dr. Cohen, is who are the community partners that one should approach?

Dr. Cohen described a pivotal shift in the conceptualization of dementia care that accompanies viewing the condition as a chronic disease. When dementia is considered a chronic condition (as outlined in Table 1), one may think more laterally and flexibly about the diversity of potential care needs, and about creating key partnerships-be they clinician/clinician partnerships or clinician/community partnerships. Such alliances can compensate for the challenges encountered in managing dementia in primary care.

Patient Needs
Patient needs are likely to include information on their diagnosis and appropriate course of treatment, educational information, supportive resources, psychological care, and decisional support as impairment increases. Inherent to the challenge of providing for these needs is that they will vary among a diverse patient population. Needs should also accord with dementia type and be tailored to each syndrome.

Many clinics are not equipped to address the full range of patient needs, and that, according to Dr. Cohen, is where community alliances help fill the breach.

Caregiver Needs
“What’s good for caregivers is good for patients,” asserted Dr. Cohen. If clinicians can help caregivers to mobilize social support, formal and informal, patient needs will also be met. The objective in meeting caregiver needs-which include education and information, social support, and assistance in mobilizing that support-is to fortify the wider circle of care around the individual with dementia.

Dr. Cohen noted that entities such as day programs, respite programs, and support groups are underused. Not only may caregivers be unaware of them, but many people do not think of themselves as caregivers and therefore do not seek out such support. They may see themselves simply as a son or daughter aiding an ailing parent. Such individuals, however, are at high risk for burnout. As Dr. Cohen described, what helps caregivers to avoid depression and burnout, will allow them to cope longer and better assist the individual with dementia. Research has shown the effectiveness of individualized plans, plans that have multiple strategies, training, information, and ongoing relationships-for the dementing illnesses may last 15 or 20 years.

Putting Dementia Care in Context
Given the foregoing, Dr. Cohen questioned how traditional care models will help the burgeoning dementia population. Dr. Cohen asked the audience to consider the broad context of dementia care. She urged listeners to “think beyond hospital walls,” to be cognizant of the “vast literature” on chronic care across many illnesses/conditions, and to recognize that many tenets for other models (diabetes, for example) will work for dementia.

An interesting model for dementia from chronic disease management is termed the “prepared practice team,” a multidisciplinary team aimed at providing broad psychosocial interventions. Supplemental strategies such as the creation of e-records, interchange of information, and coordination of team care result in an informed and empowered patient and family.

Borrowing from the Chronic Care Model

Two key parts of the chronic care model Dr. Cohen encouraged listeners to consider were facilitating self-management support and community resources (Figure 1).

Self-management could better support patients with dementia as well as their families. Self-care complements the care provided by the professional team and facilitates training to cope with the debilitating aspects of dementia, as well as promotes the use of decisional aids. Actively involving patients in their care is empowering when facing a disease bound to erode their problem-solving and decision-making capacities. Patients should be assisted in locating and using available resources and partnerships.

Disease self-management empowers individuals to become more actionable. Self-management mobilizes support, and this idea has led to the creation of programs such as cognitive memory rehabilitation services. The key, Dr. Cohen stated, is finding community resource partners to promote this kind of action. She advocates the use of case managers and family health teams. Clinicians need to ask what they can do to focus on and promote those community partnerships. Dr. Cohen used the example of an FTD daycare program at Baycrest Centre in north Toronto; she lamented that many dementia care programs are developed but underused. Patients and their caregivers need clinician encouragement to avail themselves of community programs.

Dr. Cohen suggested that clinicians might partner with caregiver resource centers, Alzheimer’s groups, and similar organizations.

Practical Suggestions for Clinicians

Dr. Cohen offered concrete suggestions for clinicians working with patients with dementia. She again advocated adopting the chronic care model for dementia. She urged them to work to better identify patient-caregiver needs. Identifying community partnerships, such as with “Meals on Wheels,” will facilitate patient care. She also urged clinicians to integrate case managers to serve as the “glue” connecting the levels of support and care.

Dr. Cohen concluded with Canadian examples of the kind of chronic care principles and community partnering she advocated. She described the FirstLink program, which is being implemented across Canada. This program provides an individual with a new dementia diagnosis a direct referral to a FirstLink clinic, which in turn gives the Alzheimer’s Society permission to call and offer available programs, services, and training. She described the founding of this program as a boon to busy MDs.

Regional networks and programs, such as the coordination of care between the Alzheimer’s Society and geriatricians in Prince Edward Island, as well as the networks of the British Columbia-based dementia clinics and community partnerships, stood out for Dr. Cohen as the kind of interventions beyond clinic walls that serves patient needs. She encouraged listeners to continue to think in these new directions, as the extent and gravity of the dementing diseases will demand the utmost of the health care system.

The Latest Research in Dementia Care: Views from the 4th Annual Canadian Colloquium on Dementia

The Latest Research in Dementia Care: Views from the 4th Annual Canadian Colloquium on Dementia

Teaser: 

Click here to view the entire report from the 4th Canadian Colloquium on Dementia

The Latest Research in Dementia Care: Views from the 4th Annual Canadian Colloquium on Dementia

The 4th Annual Canadian Colloquium on Dementia: An Overview

Speaker: Dr. Ron Keren, MD, FRCPC, 4th CCD Chair; Clinical Director, University Health Network and Whitby Mental Health Centre Memory Clinics; Assistant Professor, University of Toronto, Toronto, ON.

At present, an estimated 450,000 Canadians over 65 have Alzheimer’s disease (AD) or other related dementias. The incidence and prevalence of AD and related dementias is on the rise as the population continues to age. The expected scope and impact of the condition, and the desire to share research findings on the diagnosis and management of dementia, has led to the convening of an annual colloquium for Canadian and international dementia experts known as the Canadian Colloquium on Dementia.

The 4th Annual Canadian Colloquium on Dementia, held October 18-20, 2007 in Vancouver BC, brought together a large, expert faculty of Canadian and international speakers. The conference attracted a record number of residents and fellows compared with years past. As noted by Dr. Ron Keren, who chaired the colloquium in cooperation with co-chair Dr. Howard Feldman, the annual gathering provides a setting for exploring both clinical applications of latest research in dementia care as well as a consideration of future trends in the diagnosis and treatment of a burgeoning condition. Given both the increased attendance and record number of abstracts received by the colloquium’s organizers for the 2007 meeting, Dr. Keren described this interest in the subject as “boding well for the future of dementia care” in his opening remarks.

This report offers a closer look at select presentations from the colloquium that addressed key issues related to the diagnosis and management of dementia.

Mild Cognitive Impairment: What Is It and Where Does It Lead?

Mild Cognitive Impairment: What Is It and Where Does It Lead?

Teaser: 


Lesley J. Ritchie, MSc, Department of Psychology, Centre on Aging, University of Victoria, Victoria, BC.
Holly Tuokko, PhD, Department of Psychology, Centre on Aging, University of Victoria, Victoria, BC.

Mild cognitive impairment (MCI) is an intermediary stage in the cognitive continuum from normal aging to dementia. Six to 48% of individuals with MCI are estimated to develop dementia.1 As such, the conceptualization and operationalization of MCI present unique opportunities for the development and implementation of strategies to prevent or delay the conversion to dementia. Despite the lack of a “gold standard” case definition for MCI, information gathered from neuropsychological assessment may inform a diagnosis of MCI based on clinical judgment, as impaired performance on several neuropsychological measures is predictive of conversion to dementia for persons exhibiting cognitive decline but who are not demented.
Key words: mild cognitive impairment, dementia, conversion, neuropsychology, predictors of dementia.

The Role of the Neurologic Examination in the Diagnosis and Categorization of Dementia

The Role of the Neurologic Examination in the Diagnosis and Categorization of Dementia

Teaser: 

John R. Wherrett, MD, FRCP(C), PhD, Professor Emeritus, Division of Neurology, University of Toronto; consultant in Neurology, Toronto Western Hospital and Toronto Rehabilitation Institute; member, Memory Clinic, Toronto Western Hospital, Toronto, ON.

Nonneurologist practitioners faced with the diagnosis of dementia cannot be expected to conduct the detailed assessments for which neurologists are trained. Nonetheless, they should be able to diagnose the most common forms of neurodegenerative dementia and identify individuals that require more detailed neurologic workup. A neurologic examination algorithm is described that allows the practitioner, in a stepwise and efficient manner, to elicit findings that distinguish the main categories of neurodegenerative and vascular dementia, namely, Alzheimer’s disease, dementia with Lewy bodies, vascular dementia, and frontotemporal lobar degenerations. Patients are assessed for gait, frontal signs, signs of parkinsonism, signs of focal or lateralized lesions, neuro-ophthalmologic signs, and signs characteristic of frontotemporal lobar degeneration.
Key words: neurologic, examination, neurodegenerative, dementia, diagnosis, gait, frontal dysfunction, cognitive impairment.

Assessing Patients Complaining of Memory Impairment

Assessing Patients Complaining of Memory Impairment

Teaser: 


Mario Masellis, MSc, MD, FRCPC, Clinical Associate & Research Fellow, L.C. Campbell Cognitive Neurology Research Unit, Division of Neurology, Department of Medicine, Sunnybrook Health Sciences Centre, University of Toronto, Toronto, ON.
Sandra E. Black, MD, FRCPC, Brill Professor of Neurology, L.C. Campbell Cognitive Neurology Research Unit, Division of Neurology, Department of Medicine, Sunnybrook Health Sciences Centre, University of Toronto, Toronto, ON.

Cognitive impairment occurs along a continuum from mild subjective memory complaints occurring during the normal aging process to severe memory and other cognitive deficits due to dementia, the most common subtype being mixed Alzheimer’s disease and vascular dementia. Due to the significant growth of the older adult population, the incidence of dementia is on the rise and is posing significant challenges for health care systems worldwide. Primary care practitioners are on the front lines of this battle against dementia and will play an increasingly important role in the early identification of disease. Cognitive screening tests are helpful in detecting people in the early stages of dementia and facilitate further clinical and diagnostic evaluations. Primary care practitioners should aggressively treat known cardiovascular risk factors for dementia and institute early symptomatic therapy when appropriate.
Key words: dementia, cognitive screening test, cognitive reserve, neuroimaging, biomarkers.

Assessment of Language Function in Dementia

Assessment of Language Function in Dementia

Teaser: 


David F. Tang-Wai, MDCM, FRCPC, Assistant Professor, Department of Medicine, University of Toronto; University Health Network Memory Clinic, University of Toronto, Toronto, ON.
Naida L. Graham, PhD, Research Associate, Department of Speech-Language Pathology, University of Toronto; University Health Network Memory Clinic, University of Toronto; Toronto Rehabilitation Institute, Toronto, ON.

Impairment in language is a common finding among individuals with dementia and can be a presenting symptom, particularly in Alzheimer’s dementia and primary progressive aphasia. Early recognition of language dysfunction can help with an accurate diagnosis, management, and prognosis. There are numerous established and validated language evaluation protocols. This article provides a simple means for the primary care physician to identify and evaluate language disorders in dementia, but it is not meant to replace established protocols.
Key words: aphasia, dementia, primary progressive aphasia, semantic dementia, Alzheimer’s disease.

Depression among Older Adults with Dementia: Double Trouble

Depression among Older Adults with Dementia: Double Trouble

Teaser: 


Eran Metzger, MD, Associate Director of Geropsychiatry, Hebrew SeniorLife, Boston; Assistant Professor of Psychiatry, Harvard Medical School, Boston, MA, USA.

The management of depression among individuals with dementia can be one of the more challenging problems in geriatric practice. Depression in dementia is common regardless of the type of dementia and compounds the impairment of the underlying dementing illness. Some symptoms of dementia, including apathy, impaired concentration, and decreased food intake, may be difficult to distinguish from similar symptoms of depression. This article presents background information on the epidemiology and pathophysiology of depression in dementia followed by recommendations for a systematic approach to diagnosis. Treatment modalities including psychotherapy, pharmacotherapy, and electroconvulsive therapy are reviewed.
Key words: dementia, depression, Alzheimer’s disease, psychotherapy, psychopharmacology.

Use of Atypical Antipsychotic Medications in Later Life

Use of Atypical Antipsychotic Medications in Later Life

Teaser: 


Tarek Rajji, MD, Geriatric Mental Health Program, Centre for Addiction and Mental Health; Department of Psychiatry, University of Toronto, Toronto, ON.
Benoit H. Mulsant, MD, MSc, FRCPC, Western Psychiatric Institute and Clinic and Department of Psychiatry, University of Pittsburgh, Pittsburgh, USA; Geriatric Mental Health Program, Centre for Addiction and Mental Health; Department of Psychiatry, University of Toronto, Toronto, ON.
Hiroyuki Uchida, MD, PhD, PET Centre, Centre for Addiction and Mental Health, Toronto, ON.
David Mamo, MD, MSc, FRCPC, PET Centre and Geriatric Mental Health Program, Centre for Addiction and Mental Health; Department of Psychiatry, University of Toronto; Centre for Addiction and Mental Health, Toronto, ON.

Antipsychotics are increasingly being prescribed to older patients for the management of a variety of neuropsychiatric conditions. Available evidence supports the use of second-generation antipsychotics (SGAs) when treating these conditions. However, given their modest clinical effect for certain conditions (e.g., behavioural and psychological symptoms of dementia), their adverse effects, and their safety profile, a careful analysis of their risks and benefits is needed before initiating treatment with an SGA for an older patient. Among SGAs, choice of medication should be guided by their respective clinical indications and adverse effect profile, with use of lower initial and target doses (compared to younger adults) and periodic reviews of whether or not their continued use is warranted.
Key words: antipsychotics, older adults, dementia, delirium, schizophrenia.