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Hereditary fructose intolerance (HFI) is a genetic condition caused by a deficiency in the aldolase B enzyme. Patients with HFI are sensitive to fructose, and exposure to fructose can cause symptoms ranging from nausea to death. Treatment of HFI is currently limited to dietary restriction of fructose intake. However, emerging evidence indicates that dietary restriction is insufficient to fully protect patients from the adverse consequences of HFI. Despite strict dietary adherence, patients with HFI are more likely than the general population to develop non-alcoholic fatty liver disease and insulin resistance. This review proposes and examines evidence supporting the hypothesis that quercetin and luteolin, two inexpensive and widely available supplements, may mitigate the sequelae of HFI by inhibiting gastrointestinal fructose uptake and inhibiting endogenous fructose production. It further explores the additional hypothesis that quercetin and luteolin may mitigate the harms associated with a high-fructose diet in the general, fructose-tolerant populace. [ABSTRACT FROM AUTHOR]

Background: Traumatic brain injury (TBI) is a well‐established risk factor for Parkinson's disease (PD), though the nature of this relationship remains unclear. This study examines TBI's relationship with the AAO of and survival following PD onset among participants with PD and examines TBI's relation with PD neuropathology in an autopsy cohort. Methods: This is a retrospective observational study using the National Alzheimer's Coordinating Centers (NACC) database. TBI status was assessed based on self‐reported history. Clinicians estimate was used for determining age at onset (AAO) of cognitive decline and autopsy examination was used in assessing degree of substantia nigra neuropathology. The most recent assessment of participants was used as of June 2018, including participant visits which occurred between 2005 and 2018. The NACC dataset includes a 423 (53 TBI+) participants diagnosed with PD. Substantia nigra neuropathology was assessed in 1,133 (150 TBI+) participants, selected without regard to antemortem diagnoses. Results: TBI was associated with a 4.9 (1.5‐8.2) year earlier AAO of PD and a 5.9 (3.0‐8.8) year longer survival with PD, but not with death age or severity of substantia nigra pathology. Conclusions: TBI appears to accelerate PD onset without altering death age or PD‐related neuropathology. This relationship suggests that TBI lowers the threshold required for PD pathology to present as symptomatic PD. [ABSTRACT FROM AUTHOR]

Background: Traumatic brain injury (TBI) has been repeatedly shown to be a risk factor for several neurodegenerative diseases. However, no studies have yet examined TBI as a risk factor for corticobasal degeneration (CBD) or corticobasal syndrome (CBS), and few have examined progressive supranuclear palsy (PSP) in relation to TBI. Method: This is a retrospective observational study using the National Alzheimer's Coordinating Centers (NACC) database. TBI status was assessed based on self‐reported history. Clinicians estimate was used for determining age at onset (AAO) of cognitive decline and autopsy examination was used for neuropathological diagnosis of CBD and PSP. The most recent assessment of participants was used as of June 2018, including participant visits which occurred between 2005 and 2018. The NACC dataset includes a total of 38,249 participants. 101 (14 TBI+) participants were included with clinical (antemortem) diagnoses of PSP and 137 (16 TBI+) with CBS. 2,743 autopsy samples were also included, including 120 (14 TBI+), 58 (7 TBI+), and 11 (1 TBI+) with neuropathological (autopsy) diagnoses of PSP, CBD, or both, respectively. 181 (21 TBI+) of the participants with autopsy diagnosed PSP or CBD had antemortem cognitive decline. Result: TBI is associated with a significant 4‐year earlier AAO of cognitive decline among participants with an antemortem diagnosis of CBS and a 6‐year earlier AAO in participants with autopsy diagnosed PSP. Additionally, TBI among participants with autopsy diagnosed CBD without concomitant Alzheimer's disease (AD) neuropathology was associated with a 7‐year earlier AAO of cognitive decline (p=.066). History of TBI was not significantly associated with the prevalence of PSP and/or CBD pathology postmortem. Conclusion: This is the first report linking TBI with an earlier onset of cognitive decline in CBS and in neuropathologically defined PSP. [ABSTRACT FROM AUTHOR]