Hemodynamic changes in Alzheimer's disease: A leading role behind the courtain? Commentary on “CSF Aβ1‐42 combined with neuroimaging biomarkers in the early detection, diagnosis and prediction of Alzheimer's disease” by Lista et al.

Diomedi, Marina

doi:10.1016/j.jalz.2014.10.004

Cited by 1 publication

(2 citation statements)

References 10 publications

(15 reference statements)

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“…Truly enough, upcoming years will deal with a much more pragmatic vision of AD therapy, which explore treatable impairment such as vascular co-morbidity (Diomedi and Stefani, 2014 ) or insulin dysfunction (Wirz et al, 2014 ).…”

Section: Discussionmentioning

confidence: 99%

“…Several concomitant biochemical alterations appear to be more realistic targets. These include the malfunctioning insulin signaling (Dar et al, 2014 ; Wirz et al, 2014 ), the dysfunction of mitochondria-associated membranes, cerebrovascular changes with altered permeability (Diomedi and Stefani, 2014 ), and disturbed energy metabolism. More radically, some leaders in the functional neurosurgery world are proposing deep brain stimulation of anterior cingulate cortex (or the nucleus basalis of Meynert) (Hardenacke et al, 2013 ; Laxton and Lozano, 2013 ).…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%