Anatomical locations of the motor endplates of sartorius muscle for botulinum toxin injections in treatment of muscle spasticity.

Purpose: This study aimed to detect the idyllic locations for botulinum neurotoxin injection by analyzing the intramuscular neural distributions of the sartorius muscles.

Methods: An altered Sihler's staining was conducted on sartorius muscles (15 specimens). The nerve entry points and intramuscular arborization areas were measured as a percentage of the total distance from the most prominent point of the anterior superior iliac spine (0%) to the medial femoral epicondyle (100%).

Nec-1 alleviates cognitive impairment with reduction of Aβ and tau abnormalities in APP/PS1 mice.

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by cognitive symptoms of learning and memory deficits. Such cognitive impairments are attributed to brain atrophy resulting from progressive neuronal and synaptic loss; therefore, alleviation of neural cell death is as an important target of treatment as other classical hallmarks of AD, such as aggregation of amyloid-β (Aβ) and hyperphosphorylation of tau. Here, we found that an anti-necroptotic molecule necrostatin-1 (Nec-1) directly targets Aβ and tau proteins, alleviates brain cell death and ameliorates cognitive impairment in AD models.

Rapid and sustained cognitive recovery in APP/PS1 transgenic mice by co-administration of EPPS and donepezil.

Alzheimer's disease (AD) is a neurodegenerative disease characterized by sequential progression of pathological events, such as aggregation of amyloid-β proteins, followed by outward symptoms of cognitive impairments. Given that a combination of different therapeutic strategies often provides more rapid and effective outcomes in diverse areas of clinical treatment, we hypothesized that administration of anti-amyloid drugs with cognitive enhancers would result in synergistic effects in AD treatment. Here, we co-administered 4-(2-hydroxyethyl)-1-piperazinepropane-sulphonic acid (EPPS), an amyloid-clearing chemical, and donepezil, an acetylcholinesterase inhibitor, to determine whether they could serve complementary roles for each other in regards to AD treatment.

Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits.

Amyloid-β (Aβ) is a major pathological mediator of both familial and sporadic Alzheimer's disease (AD). In the brains of AD patients, progressive accumulation of Aβ oligomers and plaques is observed. Such Aβ abnormalities are believed to block long-term potentiation, impair synaptic function, and induce cognitive deficits.