The low-density-lipoprotein receptors represent a family of pleiotropic cell surface receptors involved in lipid homeostasis, cell migration, proliferation and differentiation. The family shares common structural features but also has significant differences mainly due to tissue-specific interactors and to peculiar proteolytic processing. Among the receptors in the family, recent studies place low-density lipoprotein receptor-related protein 8 (LRP8) at the center of both neurodegenerative and cancer-related pathways. From one side, its overexpression has been highlighted in many types of cancer including breast, gastric, prostate, lung and melanoma; from the other side, LRP8 has a potential role in neurodegeneration as apolipoprotein E (ApoE) and reelin receptor, which are, respectively, the major risk factor for developing Alzheimer’s disease (AD) and the main driver of neuronal migration, and as a γ-secretase substrate, the main enzyme responsible for amyloid formation in AD. The present review analyzes the contributions of LDL receptors, specifically of LRP8, in both cancer and neurodegeneration, pointing out that depending on various interactions and peculiar processing, the receptor can contribute to both proliferative and neurodegenerative processes.

Synucleinopathies [Parkinson’s disease (PD), dementia with Lewy bodies (DLB) and multiple system atrophy (MSA)] share filamentous α-synuclein assemblies in nerve cells and glial cells. We compared the abilities of brain extracts from MSA and PD patients to induce neuronal α-synuclein assembly and neurodegeneration following intracerebral injection in heterozygous mice transgenic for human mutant A53T α-synuclein. MSA extracts were more potent than PD extracts in inducing α-synuclein assembly and in causing neurodegeneration. MSA assemblies were Campbell-Switzer- and Gallyas-silver-positive, whereas PD assemblies were only Campbell-Switzer-positive, in confirmation of previous findings. However, induced α-synuclein inclusions were invariably Campbell-Switzer-positive and Gallyas-negative, irrespective of whether MSA or PD brain extracts were injected. The α-synuclein inclusions of non-injected homozygous mice transgenic for A53T α-synuclein were also Campbell-Switzer-positive and Gallyas-negative. These findings demonstrate that transgene expression and its intracellular environment dominated over the silver staining properties of the conformers of assembled α-synuclein.

The assembly of Tau into abundant β-sheet-rich filaments characterizes human tauopathies. A pathological pathway leading from monomeric to filamentous Tau is believed to be at the heart of these diseases. However, in Drosophila models of Tauopathy, neurodegeneration has been observed in the absence of abundant Tau filaments. Here we investigated the role of Tau assembly into β-sheets by expressing wild-type and Δ306-311 human Tau-383 in the retina and brain of Drosophila. We analyzed both lines for eye abnormalities, brain vacuolization, Tau phosphorylation and assembly, as well as climbing activity and survival. Flies expressing wild-type Tau-383 showed MC-1 staining, Tau hyperphosphorylation, and neurodegeneration. By contrast, flies expressing Δ306-311 Tau-383 had less MC-1 staining, reduced Tau hyperphosphorylation, and no detectable neurodegeneration. Their climbing ability and lifespan were similar to those of nontransgenic flies. Fluorescence spectroscopy after addition of Thioflavin T, a dye that interacts with β-sheets, showed no signal when Δ306-311 Tau-383 was incubated with heparin. These findings demonstrate that the assembly of Tau into β-sheets is necessary for neurodegeneration.

Since non-adherence to antibiotic therapy can cause several problems, including antimicrobial resistance (AMR) and treatment failures, the present study evaluated adherence to oral antibiotic therapy and AMR awareness among consecutively enrolled dental patients. Data concerning age, gender, socioeconomic status, education level, cohabitation, and general health were retrieved from medical records. AMR awareness was investigated through direct questions and adherence to antibiotic treatment was assessed through a modified Italian version of the Morisky medical scale-8 items. Participants’ characteristics were analyzed in relation to treatment adherence and AMR, using a Χ² independence test (significance level of α <0.1). Dental patients generally showed a low (51.82%) adherence to oral antibiotic therapy, and medium and high adherence was reported only by 29.37% and 18.81% of participants. Treatment adherence was similar in relation to participants’ gender and age but significantly lower in subjects with only secondary school graduation and higher in participants with higher education levels. Non-cohabitants were significantly more adherent than cohabitants. AMR awareness was declared by 42.15% of males and 38.70% of females: 56.52% of dental patients aware of AMR were 18–38 years old, 35.20% were 39–59 years old, and 26.95% were aged between 60 and 80. Further studies are needed to develop adequate strategies, expanding dental patients’ knowledge of AMR, thus optimizing the benefits and reducing the risks of antibiotic administration in dental patients.