Clinical Profile of Alzheimer’s Disease Non-Responder Patient

Martorana, Alessandro; Semprini, Roberta; Koch, Giacomo

doi:10.5772/28823

Cited by 4 publications

(4 citation statements)

References 97 publications

(65 reference statements)

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“…Thus the defect in cholinergic transmission might be due not only to the progressive neurodegeneration, but also to a more diffuse impairment of the neurotransmitter systems, in particular of the dopaminergic one (see Martorana et al, 2010). Such dysfunction could be reasonably considered responsible for executive dysfunction, a condition which predicts a change in the disease progression (Musicco et al, 2010;Martorana et al, 2011). In this view the use of drugs like rotigotine could eventually represent a valid therapeutic strategy to contrast executive dysfunction in AD cases.…”

Section: Discussionmentioning

confidence: 97%

Dopamine D2-agonist Rotigotine effects on cortical excitability and central cholinergic transmission in Alzheimer's disease patients

et al. 2013

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Section: Discussionmentioning

confidence: 97%

Dopamine D2-agonist Rotigotine effects on cortical excitability and central cholinergic transmission in Alzheimer's disease patients

et al. 2013

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“…Martorana’s group has highlighted a potential DA deficit (D1-mediated, at least in part) underlying cognitive impairment. More intriguingly, levodopa partially restored cortical transmission (evaluated by TMS tools, Martorana et al, 2008 , 2009 , 2010 , 2011 ). Levodopa and/or dopamine agonists, such as rotigotine, whose endogenous binding is not limited to D2-like preferring sites, can promote modest but significant cognitive amelioration (Martorana et al, 2013 ).…”

Section: Catecholamine Therapy In Admentioning

confidence: 99%

Catecholamine-Based Treatment in AD Patients: Expectations and Delusions

Olivola

Liguori

Hainsworth

et al. 2015

Front. Aging Neurosci.

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In Alzheimer disease, the gap between excellence of diagnostics and efficacy of therapy is wide. Despite sophisticated imaging and biochemical markers, the efficacy of available therapeutic options is limited. Here we examine the possibility that assessment of endogenous catecholamine levels in cerebrospinal fluid (CSF) may fuel new therapeutic strategies. In reviewing the available literature, we consider the effects of levodopa, monoamine oxidase inhibitors, and noradrenaline (NE) modulators, showing disparate results. We present a preliminary assessment of CSF concentrations of dopamine (DA) and NE, determined by HPLC, in a small dementia cohort of either Alzheimer’s disease (AD) or frontotemporal dementia patients, compared to control subjects. Our data reveal detectable levels of DA, NE in CSF, though we found no significant alterations in the dementia population as a whole. AD patients exhibit a small impairment of the DA axis and a larger increase of NE concentration, likely to represent a compensatory mechanism. While waiting for preventive strategies, a pragmatic approach to AD may re-evaluate catecholamine modulation, possibly stratified to dementia subtypes, as part of the therapeutic armamentarium.

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“…Moreover, in all of the studies on memantine efficacy-that is, counteracting the excitotoxic effects at glutamate synapses and also slowing down the amyloid cascade effects on cortical neurons, or for the treatment of severe dementia symptoms (in this case, it would be useful to know which symptom has to be treated with memantine)whether memantine was used because of the drug anti-NMDA profile remains unclear. Reconsidering the evaluation of memantine's efficacy would need to enroll patients considering years of disease and, as a consequence, the rate of disease progression [63][64][65][66]. Given the high diagnostic and even prognostic value of CSF biomarkers (Ab 1-42 , t-tau, and p-tau) [67][68][69][70] and PIB studies [71][72][73], their association with cognitive and functional assessment would make more reliable the evaluation of drug efficacy and also the evaluation for a more precise classification of patients (even the simple distinction between responders and nonresponders would be helpful).…”

Section: Memantine In Alzheimer's Diseasementioning

confidence: 99%

Amyloid β, Glutamate, Excitotoxicity in Alzheimer's Disease: Are We on the Right Track?

et al. 2013

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Alzheimer's disease (AD) has a devastating impact on aged people worldwide. Although sophisticated and advanced molecular methods have been developed for its diagnosis since early phases, pharmacological treatment still represents an unresolved topic. The more the disease progresses, the more the uneffectiveness of antidementia drugs emerges. New and encouraging results from experimental works indicate that glutamate pathway may play a substantial role in the pathogenesis since early stages of the disease. Several experimental data together with the clinical use of the uncompetitive N-methyl-d-aspartate (NMDA) antagonist memantine strengthen this idea. Unfortunately, definitive data on the glutamatergic transmission involvement in AD are still incomplete. Moreover, clinical results indicate only temporarily limited effects of memantine. Currently, memantine is indicated for moderate-to-severe cases of AD, an indication that may limit its efficacy and impact on Alzheimer's dementia. The association of memantine with the acetylcholinesterase inhibitor drugs used to treat dementia symptoms appears to be beneficial, in both experimental and clinical studies. Because cholinergic and glutamatergic dysfunction occurs early in AD, the coadministration of appropriate treatment in early stages of the disease might represent a valid option from the beginning of cognitive decline. Moreover, to better evaluate drug efficacy, the association of the recently introduced biomarkers with a clinical AD profile should be considered an aim to pursue.

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Clinical Profile of Alzheimer’s Disease Non-Responder Patient

Cited by 4 publications

References 97 publications

Dopamine D2-agonist Rotigotine effects on cortical excitability and central cholinergic transmission in Alzheimer's disease patients

Dopamine D2-agonist Rotigotine effects on cortical excitability and central cholinergic transmission in Alzheimer's disease patients

Catecholamine-Based Treatment in AD Patients: Expectations and Delusions

Amyloid β, Glutamate, Excitotoxicity in Alzheimer's Disease: Are We on the Right Track?

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