"haloperidol, amoxapine, etc.). The first observation linking PUFAs to abnormal movements such as dyskinesias were established in the '80s, when schizophrenic patients supplemented with a mixture of linoleic acid plus ALA or with ALA alone, which was primarily designed to alleviate their psychiatric symptoms, were also found to be less dyskinetic (Mellor et al., 1995; Vaddadi, 1984; Vaddadi et al., 1989). Haloperidolinduced motor complications in mice were similarly attenuated with high doses of DHA (Ethier et al., 2004). "
[Show abstract][Hide abstract] ABSTRACT: Current epidemiological, preclinical and clinical data suggest that omega-3 polyunsaturated fatty acids (n-3 PUFAs) may constitute therapeutic strategy for several disorders of the central nervous system, including Parkinson's disease (PD). PD is a neurodegenerative disorder primarily characterized by motor symptoms but which also includes several other pathological features such as autonomic system failures, mood disorders, and cognitive deficits. Current pharmacological options for the disease are limited to symptom management and their long-term use leads to important side effects. In this review, we discuss the evidence for the effects of n-3 PUFAs in PD both from an epidemiological perspective as well as in light of data gathered on various pathological features of the disease. Effects of n-3 PUFAs on the dopaminergic system, α-synucleinopathy, their possible mechanisms of action as well as their therapeutic potential for PD patients are also reviewed. n-3 PUFAs are inexpensive, readily transferable to the clinical setting and their use could represent a neuroprotective strategy or a disease-modifying option to delay the appearance of symptoms. It could also be beneficial as a symptomatologic treatment or serve as an add-on therapy to current pharmacological approaches. Review of the current literature as well as the undertaking of future clinical trials will shed light on these possibilities.
Ageing research reviews 03/2011; 10(4):453-63. DOI:10.1016/j.arr.2011.03.001 · 7.63 Impact Factor
"Preclinical studies have found that brain DHA concentrations are relatively resistance to loss following long-term dietary omega-3 fatty acid deficiency in the adult rat brain (Bourre et al., 1992; DeMar et al., 2004), suggesting that OFC DHA deficits may originally stem from perinatal deficits in DHA accrual that were not subsequently corrected by diet (reviewed in McNamara & Carlson, 2006). Because primate PFC DHA deficits can be normalized with long-term dietary omega-3 fatty acid treatment (Anderson et al., 2005), normalization of cortical DHA concentrations may contribute to reductions in symptom severity in SZ patients following chronic treatment with either omega-3 fatty acids (Arvindakshan et al., 2003; Emsley et al., 2002; Mellor et al., 1995; Peet et al., 2001; Peet & Horrobin, 2002) or antipsychotic medications (Arvindakshan et al., 2003; Evans et al., 2003; Khan et al., 2002). "
[Show abstract][Hide abstract] ABSTRACT: Previous studies have observed significant abnormalities in the fatty acid composition of peripheral tissues from drug-naïve first-episode schizophrenic (SZ) patients relative to normal controls, including deficits in omega-3 and omega-6 polyunsaturated fatty acids, which are partially normalized following chronic antipsychotic treatment. We hypothesized that postmortem cortical tissue from patients with SZ would also exhibit deficits in cortical docosahexaenoic acid (DHA, 22:6n-3) and arachidonic acid (AA; 20:4n-6) relative to normal controls, and that these deficits would be greater in drug-free SZ patients. We determined the total fatty acid composition of postmortem orbitofrontal cortex (OFC) (Brodmann area 10) from drug-free and antipsychotic-treated SZ patients (n=21) and age-matched normal controls (n=26) by gas chromatography. After correction for multiple comparisons, significantly lower DHA (-20%) concentrations, and significantly greater vaccenic acid (VA) (+12.5) concentrations, were found in the OFC of SZ patients relative to normal controls. Relative to age-matched same-gender controls, OFC DHA deficits, and elevated AA:DHA, oleic acid:DHA and docosapentaenoic acid (22:5n-6):DHA ratios, were found in male but not female SZ patients. SZ patients that died of cardiovascular-related disease exhibited lower DHA (-31%) and AA (-19%) concentrations, and greater OA (+20%) and VA (+17%) concentrations, relative to normal controls that also died of cardiovascular-related disease. OFC DHA and AA deficits, and elevations in oleic acid and vaccenic acid, were numerically greater in drug-free SZ patients and were partially normalized in SZ patients treated with antipsychotic medications (atypical>typical). Fatty acid abnormalities could not be wholly attributed to lifestyle or postmortem tissue variables. These findings add to a growing body of evidence implicating omega-3 fatty acid deficiency as well as the OFC in the pathoaetiology of SZ, and suggest that abnormalities in OFC fatty acid composition may be gender-specific and partially normalized by antipsychotic medications.
Schizophrenia Research 04/2007; 91(1-3):37-50. DOI:10.1016/j.schres.2006.11.027 · 4.43 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The neurodevelopmental hypothesis of schizophrenia is becoming an important feature of research in the field. However, its major drawback is that it lacks any biochemical basis which might draw the diverse observations together. It is suggested that the membrane phospholipid hypothesis can provide such a biochemical basis and that the neurodevelopmental phospholipid concept offers a powerful paradigm to guide future research.
Schizophrenia Research 05/1998; 30(3):193-208. DOI:10.1016/S0920-9964(97)00151-5 · 4.43 Impact Factor
Note: This list is based on the publications in our database and might not be exhaustive.
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.