Introduction Iron accumulates in the brain during aging, which catalyzes radical formation, causing neuronal impairment, and is thus considered a pathogenic factor in Alzheimer's disease (AD). To scavenge excess iron‐catalyzed radicals and thereby protect the brain and decrease the incidence of AD, we synthesized a soluble pro‐iron 5‐YHEDA peptide. However, the blood‐brain barrier (BBB) blocks large drug molecules from entering the brain and thus strongly reduces their therapeutic effects. However, alternative receptor‐ or transporter‐mediated approaches are possible. Methods A low‐density lipoprotein receptor (LDLR)‐binding segment of Apolipoprotein B‐100 was linked to the 5‐YHEDA peptide (bs‐5‐YHEDA) and intracardially injected into senescent (SN) mice that displayed symptoms of cognitive impairment similar to those of people with AD. Results We successfully delivered 5‐YHEDA across the BBB into the brains of the SN mice via vascular epithelium LDLR‐mediated endocytosis. The data showed that excess brain iron and radical‐induced neuronal necrosis were reduced after the bs‐5‐YHEDA treatment, together with cognitive amelioration in the SN mouse, and that the senescence‐associated ferritin and transferrin increase, anemia and inflammation reversed without kidney or liver injury. Discussion bs‐5‐YHEDA may be a mild and safe iron remover that can cross the BBB and enter the brain to relieve excessive iron‐ and radical‐induced cognitive disorders.

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Alzheimer's disease (AD) is currently incurable and places a large burden on the caregivers of AD patients. In the AD brain, iron is abundant, catalyzing free radicals and impairing neurons. The blood-brain barrier hampers antidementia drug delivery via circulation to the brain, which limits the therapeutic effects of drugs. Here, according to the method described by Gobinda, we synthesized a 16 lysine (K) residue-linked low-density lipoprotein receptor-related protein (LRP)-binding amino acid segment of apolipoprotein E (K16APoE). By mixing this protein with our designed therapeutic peptide HAYED, we successfully transported HAYED into an AD model mouse brain, and the peptide scavenged excess iron and radicals and decreased the necrosis of neurons, thus easing AD.

Background: The idea of remotely manipulating other people or animals without contact or invasion has existed long time ago. Many people have tried, but no one really make it happen. Recently, the technique of Brain-Computer interfacing is mushrooming. It was said researchers had partially realized the direct communication with brain and even the manipulation of the subject's behavior via a chip embedded in the brain. Nevertheless, for the trauma of implantation, such chip-intrusive method is not favorite to the healthy people. Objective: To explore a contactless and noninvasive technique to remotely manipulate the consciousness and behaviors of animals or humans. Methods: The anesthetized mice or sciatic nerve samples were caged in an air-filled bottle and set as the target. A pulsed intense-field laser (PIFL) beam (λ=532 nm; P=20 TW; E=0.1 J/cm 2 ; pulse width=30 fs; f=1 Hz) was emitted to the targets 1.2 m away. Results: θ-Rhythm mouse brain waves were evoked and recorded, and potentials in the detached frog sciatic nerve were stimulated without contact or invasion. Conclusion: The experiments shown that Pulsed Intense-field Lasers can evoke EEG and potentials in nerves contactlessly and noninvasively. It inspired us that we can remotely manipulate consciousness or behaviors on animals or humans by PIFL, which might bring about development to the Information Science and provide new medical treatment.

Alzheimer's disease (AD) is a progressive neurodegenerative disease characterized by 11 memory and cognitive decline. It is incurable currently and places a great burden on the caregivers of 12 patients. Iron is rich in the brain of AD suffers. It catalyzes radicals which impairs neurons. Therefore,