Lecithin for dementia and cognitive impairment

PLD1-Dependent Regulation of Synaptic Integrity: Implications for Cognitive Resilience and Alzheimer’s Disease Pathogenesis

“…We established clinical relevance by discovering aberrant overexpression of PLD1, but not PLD2 in crude synaptoneurosomal fractions from post-mortem AD patients hippocampal tissues compared to age-matched controls (Krishnan et al 2018). This observation was corroborated by findings of upregulated PLD1 immunoreactivity in reactive astrocytes surrounding amyloid plaques in AD brains (Jin et al 2007) and supported by historical reports of generally elevated PLD activity in AD (Kanfer et al 1996; Higgins & Flicker 2000). Consistent with such human data, we identified an age-dependent increase in the crude synaptoneurosomal fractions of hippocampal PLD1 in the late-onset 3xTg-AD mouse model (Oddo et al 2003; Javonillo et al 2022), which recapitulates key aspects of both amyloid-β (Aβ) and tau pathology (Krishnan et al 2018), where this widely used transgenic model harbors human transgenes for mutant Amyloid Precursor Protein (APP Swe ), Presenilin-1 (PS1 M146V ), and microtubule-associated protein tau (MAPT P301L ) (Barber et al 2023).…”

PLD1-Dependent Regulation of Synaptic Integrity: Implications for Cognitive Resilience and Alzheimer’s Disease Pathogenesis

“…We established clinical relevance by discovering aberrant overexpression of PLD1, but not PLD2 in crude synaptoneurosomal fractions from post-mortem AD patients hippocampal tissues compared to age-matched controls (Krishnan et al 2018). This observation was corroborated by findings of upregulated PLD1 immunoreactivity in reactive astrocytes surrounding amyloid plaques in AD brains (Jin et al 2007) and supported by historical reports of generally elevated PLD activity in AD (Kanfer et al 1996; Higgins & Flicker 2000). Consistent with such human data, we identified an age-dependent increase in the crude synaptoneurosomal fractions of hippocampal PLD1 in the late-onset 3xTg-AD mouse model (Oddo et al 2003; Javonillo et al 2022), which recapitulates key aspects of both amyloid-β (Aβ) and tau pathology (Krishnan et al 2018), where this widely used transgenic model harbors human transgenes for mutant Amyloid Precursor Protein (APP Swe ), Presenilin-1 (PS1 M146V ), and microtubule-associated protein tau (MAPT P301L ) (Barber et al 2023).…”

Nootropics as Cognitive Enhancers: Types, Dosage and Side Effects of Smart Drugs

“…In contrast, results from randomized in vivo studies have shown no benefit of lecithin in treating patients with Alzheimer's and Parkinson's disease [163]. The data suggest that a lack of control over the subject's learning levels may contribute to inconsistent findings.…”

Rapid Biomarker Screening of Alzheimer’s Disease by Interpretable Machine Learning and Graphene-Assisted Raman Spectroscopy

“…Banks et al also showed that the decrease of triglycerides improves both learning and memory capabilities . Additionally, phosphatidylcholine is found to be significantly lower in AD patients, where high levels of phosphatidylcholine usually reduce the progression of dementia . However, it is worth noting that the AD pathogenesis is different in mice and human brains in terms of the phosphatidylcholine level.…”

“…68 Additionally, phosphatidylcholine is found to be significantly lower in AD patients, 71 where high levels of phosphatidylcholine usually reduce the progression of dementia. 72 However, it is worth noting that the AD pathogenesis is different in mice and human brains in terms of the phosphatidylcholine level. According to Chan et al, phosphatidylcholine levels are lower in the AD human brain but higher in the mouse forebrain (18 mol% for AD animals and 16 mol% for healthy animals).…”

PLD1-Dependent Regulation of Synaptic Integrity: Implications for Cognitive Resilience and Alzheimer’s Disease Pathogenesis

“…We established clinical relevance by discovering aberrant overexpression of PLD1, but not PLD2 in crude synaptoneurosomal fractions from post-mortem AD patients hippocampal tissues compared to age-matched controls (Krishnan et al 2018). This observation was corroborated by findings of upregulated PLD1 immunoreactivity in reactive astrocytes surrounding amyloid plaques in AD brains (Jin et al 2007) and supported by historical reports of generally elevated PLD activity in AD (Kanfer et al 1996; Higgins & Flicker 2000). Consistent with such human data, we identified an age-dependent increase in the crude synaptoneurosomal fractions of hippocampal PLD1 in the late-onset 3xTg-AD mouse model (Oddo et al 2003; Javonillo et al 2022), which recapitulates key aspects of both amyloid-β (Aβ) and tau pathology (Krishnan et al 2018), where this widely used transgenic model harbors human transgenes for mutant Amyloid Precursor Protein (APP Swe ), Presenilin-1 (PS1 M146V ), and microtubule-associated protein tau (MAPT P301L ) (Barber et al 2023).…”

Nootropics as Cognitive Enhancers: Types, Dosage and Side Effects of Smart Drugs

“…In contrast, results from randomized in vivo studies have shown no benefit of lecithin in treating patients with Alzheimer's and Parkinson's disease [163]. The data suggest that a lack of control over the subject's learning levels may contribute to inconsistent findings.…”

Rapid Biomarker Screening of Alzheimer’s Disease by Interpretable Machine Learning and Graphene-Assisted Raman Spectroscopy

“…Banks et al also showed that the decrease of triglycerides improves both learning and memory capabilities . Additionally, phosphatidylcholine is found to be significantly lower in AD patients, where high levels of phosphatidylcholine usually reduce the progression of dementia . However, it is worth noting that the AD pathogenesis is different in mice and human brains in terms of the phosphatidylcholine level.…”

“…68 Additionally, phosphatidylcholine is found to be significantly lower in AD patients, 71 where high levels of phosphatidylcholine usually reduce the progression of dementia. 72 However, it is worth noting that the AD pathogenesis is different in mice and human brains in terms of the phosphatidylcholine level. According to Chan et al, phosphatidylcholine levels are lower in the AD human brain but higher in the mouse forebrain (18 mol% for AD animals and 16 mol% for healthy animals).…”

PLD1-Dependent Regulation of Synaptic Integrity: Implications for Cognitive Resilience and Alzheimer’s Disease Pathogenesis

“…We established clinical relevance by discovering aberrant overexpression of PLD1, but not PLD2 in crude synaptoneurosomal fractions from post-mortem AD patients hippocampal tissues compared to age-matched controls (Krishnan et al 2018). This observation was corroborated by findings of upregulated PLD1 immunoreactivity in reactive astrocytes surrounding amyloid plaques in AD brains (Jin et al 2007) and supported by historical reports of generally elevated PLD activity in AD (Kanfer et al 1996; Higgins & Flicker 2000). Consistent with such human data, we identified an age-dependent increase in the crude synaptoneurosomal fractions of hippocampal PLD1 in the late-onset 3xTg-AD mouse model (Oddo et al 2003; Javonillo et al 2022), which recapitulates key aspects of both amyloid-β (Aβ) and tau pathology (Krishnan et al 2018), where this widely used transgenic model harbors human transgenes for mutant Amyloid Precursor Protein (APP Swe ), Presenilin-1 (PS1 M146V ), and microtubule-associated protein tau (MAPT P301L ) (Barber et al 2023).…”

Nootropics as Cognitive Enhancers: Types, Dosage and Side Effects of Smart Drugs

“…In contrast, results from randomized in vivo studies have shown no benefit of lecithin in treating patients with Alzheimer's and Parkinson's disease [163]. The data suggest that a lack of control over the subject's learning levels may contribute to inconsistent findings.…”

Rapid Biomarker Screening of Alzheimer’s Disease by Interpretable Machine Learning and Graphene-Assisted Raman Spectroscopy

“…Banks et al also showed that the decrease of triglycerides improves both learning and memory capabilities . Additionally, phosphatidylcholine is found to be significantly lower in AD patients, where high levels of phosphatidylcholine usually reduce the progression of dementia . However, it is worth noting that the AD pathogenesis is different in mice and human brains in terms of the phosphatidylcholine level.…”

“…68 Additionally, phosphatidylcholine is found to be significantly lower in AD patients, 71 where high levels of phosphatidylcholine usually reduce the progression of dementia. 72 However, it is worth noting that the AD pathogenesis is different in mice and human brains in terms of the phosphatidylcholine level. According to Chan et al, phosphatidylcholine levels are lower in the AD human brain but higher in the mouse forebrain (18 mol% for AD animals and 16 mol% for healthy animals).…”