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Claudia Jacova

Publications and source records attributed to Claudia Jacova.

5 recordsLinked to original sources
PubMed2006

Dropouts and refusals in observational studies: lessons for prevention trials.

The success of prevention trials of Alzheimer disease and other dementias (AD/dementia) hinges on their ability to recruit and retain at-risk study populations. Losing subjects is a threat to the power to detect a treatment effect and, potentially, to the validity of these studies. Observational cohort studies accumulate data around participant outcomes that can help to inform the design of future prevention trials. Our objectives were to investigate the rates of refusal and dropout within observational cohort studies and to evaluate their characteristics and impact. This study examined data from the Canadian Cohort Study of Cognitive Impairment and Related Dementias (ACCORD), a 2-year observational cohort study of patients newly referred to dementia clinics. The sample included 124 Not Cognitively Impaired (NCI) and 342 Cognitively Impaired Not Demented (CIND) subjects. Subjects who refused initial neuropsychological (NP) testing were compared to those who completed NP testing and subjects who dropped out to those who attended follow-up. Refusal was common, with 40% of subjects not completing neuropsychological testing at baseline. Dropout was also substantial, with 55% lost to the 2-year follow-up. Subjects who refused NP testing were significantly older and less educated. CIND refusers had lower cognitive and functional scores at entry and a 2-year progression rate to dementia twice as high as that of non-refusers. CIND dropouts also had lower baseline cognitive and functional scores. These observations suggest that dropouts and refusals in prevention trials include those subjects who are at high risk for progression to AD/dementia. Targeted strategies to retain these individuals within prevention studies will be needed to achieve sufficient study power and validity.

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PubMed2006

Clinical practice with anti-dementia drugs: a consensus statement from British Association for Psychopharmacology.

The British Association for Psychopharmacology (BAP) coordinated a meeting of experts to review the evidence on the drug treatment for dementia. The level of evidence (types) was rated using a standard system: Types 1a and 1b (evidence from meta-analysis of randomised controlled trials or at least one controlled trial respectively); types 2a and 2b (one well-designed study or one other type of quasi experimental study respectively); type 3 (non-experimental descriptive studies); and type 4 (expert opinion). There is type 1a evidence for cholinesterase inhibitors (donepezil, rivastigmine and galantamine) for mild to moderate Alzheimer's disease; memantine for moderate to severe Alzheimer's disease; and for the use of bright light therapy and aromatherapy. There is type 1a evidence of no effect of anti inflammatory drugs or statins. There is conflicting evidence regarding oestrogens, with type 2a evidence of a protective effect of oestrogens but 1b evidence of a harmful effect. Type 1a evidence for any effect of B12 and folate will be forthcoming when current trials report. There is type 1b evidence for gingko biloba in producing a modest benefit of cognitive function; cholinesterase inhibitors for the treatment of people with Lewy body disease (particularly neuropsychiatric symptoms); cholinesterase inhibitors and memantine in treatment cognitive impairment associated with vascular dementia; and the effect of metal collating agents (although these should not be prescribed until more data on safety and efficacy are available). There is type 1b evidence to show that neither cholinesterase inhibitors nor vitamin E reduce the risk of developing Alzheimer's disease in people with mild cognitive impairment; and there is no evidence that there is any intervention that can prevent the onset of dementia. There is type 1b evidence for the beneficial effects of adding memantine to cholinesterase inhibitors, and type 2b evidence of positive switching outcomes from one cholinesterase inhibitor to another. There is type 2a evidence for a positive effect of reminiscence therapy, and type 2a evidence that cognitive training does not work. There is type 3 evidence to support the use of psychological interventions in dementia. There is type 2 evidence that a clinical diagnosis of dementia can be made accurately and that brain imaging increases that accuracy. Although the consensus statement dealt largely with medication, the role of dementia care in secondary services (geriatric medicine and old age psychiatry) and primary care, along with health economics, was discussed. There is ample evidence that there are effective treatments for people with dementia, and Alzheimer's disease in particular. Patients, their carers, and clinicians deserve to be optimistic in a field which often attracts therapeutic nihilism.

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PubMed2005

Mild cognitive impairment.

Mild cognitive impairment (MCI) describes a state of cognitive functioning that is below defined norms, yet falls short of dementia in severity. It exists across a cognitive continuum with borders that are difficult to define precisely. Within our "graying" western societies, its prevalence increases with age. A number of subtypes of MCI, including age-associated memory impairment (AAMI), age-associated cognitive decline (AACD), amnestic MCI (MCIa), and cognitive impairment not dementia (CIND) have contributed to our understanding of MCI. Recent efforts have been directed at developing a uniform diagnostic classification for MCI that reflects the maturation of knowledge about this state. There is considerable etiological and clinical heterogeneity within MCI; however, there is a unifying increased risk of progression to dementia. The diagnostic process for MCI involves assessment of multiple cognitive domains, with particular attention to episodic and semantic memory, while neuroimaging with structural MRI and PET both add to the diagnostic and prognostic evaluation of MCI. Although there are no pharmacological treatments at present that are capable of delaying the long-term progression of MCI to dementia, there is some evidence of short-term symptomatic benefits with acetylcholinesterase inhibitors. MCI is an important clinical problem, which clinicians can expect to face with increasing frequency. The essentials of management include a thorough assessment directed at etiological determination and counseling and judicious use of available therapeutics.

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PubMed2004

Some pitfalls in measuring memory in animals.

Because the presence or absence of memories in the brain cannot be directly observed, scientists must rely on indirect measures and use inferential reasoning to make statements about the status of memories. In humans, memories are often accessed through spoken or written language. In animals, memory is accessed through overt behaviours such as running down an arm in a maze, pressing a lever, or visiting a food cache site. Because memory is measured by these indirect methods, errors in the veracity of statements about memory can occur. In this brief paper, we identify three areas that may serve as pitfalls in reasoning about memory in animals: (1) the presence of 'silent associations', (2) intrusions of species-typical behaviours on memory tasks, and (3) improper mapping between human and animals memory tasks. There are undoubtedly other areas in which scientists should act cautiously when reasoning about the status of memory.

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