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Alzheimer's disease (AD) is the most prevalent form of dementia and is characterized by progressive degeneration of brain function. AD gradually affects the parts of the brain that control thoughts, language, behavior and mental function, severely impacting a person's ability to carry out daily activities and ultimately leading to death. The accumulation of extracellular amyloid-β peptide (Aβ) and the aggregation of intracellular hyperphosphorylated tau are the two key pathological hallmarks of AD. AD is a complex condition that involves both non-genetic risk factors (35%) and genetic risk factors (58-79%). The glymphatic system plays an essential role in clearing metabolic waste, transporting tissue fluid, and participating in the immune response. Both non-genetic and genetic risk factors affect the glymphatic system to varying degrees. The main purpose of this review is to summarize the underlying mechanisms involved in the deregulation of the glymphatic system during the progression of AD, especially concerning the diverse contributions of non-genetic and genetic risk factors. In the future, new targets and interventions that modulate these interrelated mechanisms will be beneficial for the prevention and treatment of AD.

Aim: To investigate the regulatory network of hippocampal-systemic arterial blood pressure during epileptic network reestablishment., Methods: 7.2 microg picrotoxin (PTX) was microinjected into the right HPC (RHPC) to induce rat epilepsy. Contralateral hippocampal EEG, single unit discharges, femoral artery blood pressure and ECG were recorded simultaneously., Results: PTX might induce: (1) A resemblance interspike intervals (ISI) spot distribution of long duration neuronal burst and unit after discharges in contralateral HPC. (2) Delayed the initiation time of hippocampal neuronal bursts coupled with arterial blood pressure depression. (3) Hippocampal neuronal burst or unit after discharges coupled complexly with arterial blood pressure depression. (4) Resemblance hippocampal EEG interpeak intervals (IPI) and neuronal firing ISI spot distribution coupled with arterial blood pressure depression., Conclusion: During contralateral hippocampal epileptic network reestablishment after microinjection of PTX to the RHPC, the function of the hippocampal-arterial blood pressure regulatory network could be modulated by characteristic network and neuronal temporal code patterning.

Aim: The electrographic and behavioral kindling effects were induced by chronic tetanization of the right caudate-putamen (CPu) to study the target-behavior expression involved in the CPu or hippocampus (HPC) network abnormalities., Methods: Experiments were performed on 58 SD rats. Tetanization (60Hz,0.4 - 0.6mA, 2s) was delivered into the CPu or the HPC, once a day, for 7-12 days. Animal behaviors were observed every day and depth electrographs were recorded at the beginning or at the end of the experiments., Results: Chronic tetanization of the CPu or of the HPC induced: (1) Rhythmic sharp waves in the CPu and paroxysmal epileptiform events in the HPC electrographs. (2) Primary behavioral seizures, secondary behavioral seizures, and kindling effects, including wet dog shakes (WEDS), rearing, face washing, immobility, chewing and head nodding. (3) Lower rate of primary WEDS (P < 0.01), and higher rate of secondary WEDS (P < 0.01) in the CPu-tetanized rats. (4) Longer silent period of behavioral seizures before kindling appeared in the CPu-tetanized rats., Conclusion: Kindling effects in the CPu-tetanized rats resembles those in the HPC-tetanized rats. The CPu might participate in the origin of epileptic focus and be involved in reestablishment of limbic epileptic networks, which may be responsible for the target-behavioral seizures.