Serum folate concentrations in patients with cortical and subcortical dementias

Lovati, Carlo; Galimberti, Daniela; Pomati, Simone; Capiluppi, E.; Dolci, Alberto; Scapellato, Luisa; Rosa, Sílvia Aguiar; Mailland, Enrico; Suardelli, Massimo; Vanotti, Alfredo; Clerici, Francesca; Santarato, Donatella; Panteghini, Mauro; Scarpini, Elio; Mariani, Claudio; Bertora, Pierluigi

doi:10.1016/j.neulet.2007.04.060

Cited by 12 publications

(7 citation statements)

References 19 publications

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“…2 Low serum folate levels in FTD patients have been previously described. 3 In the present case, an increased MMSE score was observed after folic acid treatment, which is consistent with a previous report of reversing cognitive impairment. 4 In contrast, there is disagreement regarding the association between folate deficiency and FTD.…”

Section: Discussionsupporting

confidence: 93%

A case of folate deficiency showing behavioural variant of frontotemporal dementia‐like symptoms

Fujii,

Ikenouchi,

Okamoto

et al. 2023

Psychogeriatrics

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Section: Discussionsupporting

confidence: 93%

A case of folate deficiency showing behavioural variant of frontotemporal dementia‐like symptoms

Fujii,

Ikenouchi,

Okamoto

et al. 2023

Psychogeriatrics

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“…Among the many hypotheses on the pathogenesis of Alzheimer's disease (AD) being tested, virtually none provide a unifying insight on the seemingly diverse early events that trigger the putative metabolic and cellular alterations that precede neuronal degeneration [3,8]. In fact, virtually none of them provide a well articulated, cogent reason why factors as diverse as head injury, high fat intake, B vitamin deficiency [4,7], central nervous system infections [6], alterations in cholesterol homeostasis [13,15] and many others, increase the risk of developing the disorder, whereas none of these risk factors seem to act as true causative factors. For example, the most commonly held amyloid hypothesis rests on the concept that the amyloid-β peptide, Aβ 1−42 , self-polymerizes over years to eventually form senile plaques, which are thus putatively responsible for the entire array of subsequent brain lesions.…”

Section: Neuroimmunomodulation Hypothesismentioning

confidence: 99%

“…The resulting inflammatory cytokines in all of these situations can play a dual role, either promoting neurodegeneration or assisting neuroprotection [12]. Thus, if pro-inflammatory mediators were simply protective, one should expect that individuals receiving NSAIDs would be at higher risk of AD, which appears not to be the case [7,16]. In fact, the evidence indicates that only few proinflammatory molecules, such as tumor necrosis factor-α (TNF-α) [16], exert neuroprotective effects.…”

Section: Neuroimmunomodulation Hypothesismentioning

confidence: 99%

The Damage Signals Hypothesis of Alzheimer's Disease Pathogenesis

Fernández

Rojo

Kuljiš

et al. 2008

JAD

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Virtually none of the hypotheses on Alzheimer's disease (AD) pathogenesis address the earliest events that trigger the molecular alterations that precede cerebral degeneration and account for the diversity of risk factors that converge on a well-defined disease phenotype. We propose that long-term activation of the innate immune system by an individual array of risk factors constitutes a unifying mechanism leading to the triggering of an inflammatory cascade that converges in cytoskeletal alterations (tau aggregation, paired helical filament formation) as a previously hypothesized final common pathway in AD. The key pathogenic phenomena consist in the long-term, maladaptive activation of innate immunity-triggering receptors -such as the toll-like and advanced glycation end-products receptors, and others located in the microglial membrane -by seemingly heterogeneous risk factors such as hyperlipidemia, hyperglycemia, oxidative stress, head injury, amyloid oligomers, etc. Our hypothesis provides a unifying mechanism that explains both the diversity of risk factors acting over long periods of time and the individual response to such insults. This formulation is amenable to both empirical testing and implementation into therapeutic strategies that may lead to effective prevention of AD as well as other disorders in which impaired regulation of the innate immunity is the unifying cause of the condition.

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“…In mouse models, folate deficiency has been demonstrated to decrease neurotransmitter acethylcholine activity, which in turn significantly decreases cognitive performance [72]. Furthermore, low serum folate concentrations were also found in patients with Alzheimer’s disease and dementia [73]. There is also evidence of the beneficiary effect of folate therapy on both EEG patterns and neuropsychological performance in patients with neuropathy and cerebral atrophy [74].…”

Section: Discussionmentioning

confidence: 99%

Metabolomic Profiling of Cerebral Palsy Brain Tissue Reveals Novel Central Biomarkers and Biochemical Pathways Associated with the Disease: A Pilot Study

et al. 2019

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Cerebral palsy (CP) is one of the most common causes of motor disability in childhood, with complex and heterogeneous etiopathophysiology and clinical presentation. Understanding the metabolic processes associated with the disease may aid in the discovery of preventive measures and therapy. Tissue samples (caudate nucleus) were obtained from post-mortem CP cases (n = 9) and age- and gender-matched control subjects (n = 11). We employed a targeted metabolomics approach using both 1H NMR and direct injection liquid chromatography-tandem mass spectrometry (DI/LC-MS/MS). We accurately identified and quantified 55 metabolites using 1H NMR and 186 using DI/LC-MS/MS. Among the 222 detected metabolites, 27 showed significant concentration changes between CP cases and controls. Glycerophospholipids and urea were the most commonly selected metabolites used to develop predictive models capable of discriminating between CP and controls. Metabolomics enrichment analysis identified folate, propanoate, and androgen/estrogen metabolism as the top three significantly perturbed pathways. We report for the first time the metabolomic profiling of post-mortem brain tissue from patients who died from cerebral palsy. These findings could help to further investigate the complex etiopathophysiology of CP while identifying predictive, central biomarkers of CP.

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Serum folate concentrations in patients with cortical and subcortical dementias

Cited by 12 publications

References 19 publications

A case of folate deficiency showing behavioural variant of frontotemporal dementia‐like symptoms

A case of folate deficiency showing behavioural variant of frontotemporal dementia‐like symptoms

The Damage Signals Hypothesis of Alzheimer's Disease Pathogenesis

Metabolomic Profiling of Cerebral Palsy Brain Tissue Reveals Novel Central Biomarkers and Biochemical Pathways Associated with the Disease: A Pilot Study

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