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Articles by Jeffrey L. Cummings
Total Records ( 4 ) for Jeffrey L. Cummings
  Jeffrey L. Cummings
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  Jeffrey L. Cummings
  Alzheimer's disease (AD) might be treated with symptomatic, neuroprotective, or neurorestorative therapies. Neuroprotective and neurorestorative interventions are disease-modifying therapies. Disease modification can be defined as treatments or interventions that affect the underlying pathophysiology of the disease and have a beneficial outcome on the course of AD. In a clinical trial the criteria for affecting the underlying cause of the disease can be supported by demonstrating an effect on a biomarker such as medial temporal atrophy on magnetic resonance imaging (MRI) or diminished tau or phospho-tau levels in cerebrospinal fluid. The claim for a beneficial effect on the clinical course of AD is supported by a drug-placebo difference on the primary clinical outcomes of the clinical trial. A statistically significant correlation between the biomarker outcome and the clinical trial outcome would support the claim that these are based on the same underlying mechanism. Delayed start or staggered withdrawal designs might in themselves support a disease-modifying claim but are difficult to implement. A combination of clinical outcomes and biomarker measures is a more likely pathway to a disease-modifying claim. Labeling of disease-modifying agents might refer to slowing of disease progression, delay in reaching predefined disease milestones, or reduction in progression of a biomarker such as cerebral atrophy or ventricular enlargement on MRI. Prevention claims will depend heavily on biomarker outcomes.
  Zuzana Walker and Jeffrey L. Cummings
  Early, accurate diagnosis of dementia with Lewy bodies (DLB), in particular its differentiation from Alzheimer‘s disease, is important for optimal management, providing patients/carers with information about the likely symptomatology and illness course, allowing initiation of effective pharmacotherapy, and avoiding the consequences of neuroleptic sensitivity. Clinical diagnosis of DLB has high specificity but low sensitivity. Clinical trials of [123I]N-ω-fluoropropyl-2β-carbomethoxy-3β-(4-iodophenyl)nortropane single-photon emission computed tomography ([123I]FP-CIT SPECT) indicate high positive and negative percent agreement with reference to clinical diagnosis, and high sensitivity and specificity in patients with neuropathologically confirmed diagnoses of DLB. An abnormal [123I]FP-CIT SPECT image in patients fulfilling criteria for possible DLB advances the certainty of a diagnosis to probable DLB. [123I]FP-CIT SPECT, by identifying the striatal dopaminergic deficit, can be a valuable diagnostic aid and can provide support to a clinical diagnosis of DLB in patients with dementia. The technique is likely to be of particular utility in patients with dementia with an uncertain diagnosis.
  Adam L. Boxer , Michael Gold , Edward Huey , William T. Hu , Howard Rosen , Joel Kramer , Fen-Biao Gao , Edward A. Burton , Tiffany Chow , Aimee Kao , Blair R. Leavitt , Bruce Lamb , Megan Grether , David Knopman , David Knopman , Ian R. Mackenzie , Laura Mitic , Erik D. Roberson , Daniel Van Kammen , Marc Cantillon , Kathleen Zahs , George Jackson , Stephen Salloway , John Morris , Gary Tong , Howard Feldman , Howard Fillit , Susan Dickinson , Zaven S. Khachaturian , Margaret Sutherland , Susan Abushakra , Joseph Lewcock , Robert Farese , Robert O. Kenet , Frank LaFerla , Steve Perrin , Steve Whitaker , Lawrence Honig , Marsel M. Mesulam , Brad Boeve , Murray Grossman , Bruce L. Miller and Jeffrey L. Cummings
  Frontotemporal degeneration (FTD) encompasses a spectrum of related neurodegenerative disorders with behavioral, language, and motor phenotypes for which there are currently no effective therapies. This is the second of two articles that summarize the presentations and discussions that occurred at two symposia in 2011 sponsored by the Frontotemporal Degeneration Treatment Study Group, a collaborative group of academic and industry researchers that is devoted to developing treatments for FTD. This article discusses the current status of FTD clinical research that is relevant to the conduct of clinical trials, and why FTD research may be an attractive pathway for developing therapies for neurodegenerative disorders. The clinical and molecular features of FTD, including rapid disease progression and relatively pure molecular pathology, suggest that there are advantages to developing drugs for FTD as compared with other dementias. FTD qualifies as orphan indication, providing additional advantages for drug development. Two recent sets of consensus diagnostic criteria will facilitate the identification of patients with FTD, and a variety of neuropsychological, functional, and behavioral scales have been shown to be sensitive to disease progression. Moreover, quantitative neuroimaging measurements demonstrate progressive brain atrophy in FTD at rates that may surpass Alzheimer's disease. Finally, the similarities between FTD and other neurodegenerative diseases with drug development efforts already underway suggest that FTD researchers will be able to draw on this experience to create a road map for FTD drug development. We conclude that FTD research has reached sufficient maturity to pursue clinical development of specific FTD therapies.
 
 
 
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