Related Experiment Video
Updated: May 27, 2026

08:01
Intracerebroventricular Injection of Amyloid-β Peptides in Normal Mice to Acutely Induce Alzheimer-like Cognitive Deficits
Published on: March 16, 2016
Repositioning leptin as a therapy for Alzheimer's disease
Jane M Johnston1, Steven J Greco, Ashkan Hamzelou
1Neurotez, Inc., 991 Highway 22, Suite 200A Bridgewater, NJ 08807, USA.
Summary
Recombinant human leptin, initially for obesity, shows long-term safety and cognitive benefits. Emerging data suggest leptin therapy may be a promising treatment for Alzheimer
Area of Science:
- Endocrinology and Metabolism
- Neuroscience and Neurology
- Pharmacology
Background:
- Recombinant human leptin (rhLeptin) trials for obesity began in 1998.
- Subsequent research explored rhLeptin's dosage, safety, and efficacy across diverse patient groups.
- Leptin's neuroprotective and cognitive functions remain underappreciated.
Purpose of the Study:
- To review current clinical trial data on leptin therapy.
- To assess the long-term safety of leptin administration in humans.
- To summarize reported cognitive benefits and explore potential therapeutic applications, particularly for Alzheimer's disease.
Main Methods:
- Comprehensive review of existing clinical trial data on leptin therapy.
- Analysis of safety, dosage, and efficacy studies in pediatric and adult subjects.
- Synthesis of evidence regarding leptin's effects on cognition and neuroprotection.
Main Results:
- Leptin administration is demonstrated to be safe for long-term human use.
- Reported cognitive benefits associated with leptin therapy are summarized.
- Accumulating data indicate a significant potential for leptin as an Alzheimer's disease therapy.
Conclusions:
- Leptin therapy is safe for long-term use and offers cognitive benefits.
- The neuroprotective and cognitive roles of leptin warrant further investigation.
- Leptin presents a promising therapeutic avenue for Alzheimer's disease.
Related Concept Videos
Alzheimer's Disease: Treatment
Alzheimer's Disease (AD), a neurodegenerative disorder, is pathologically identified by amyloid plaques and neurofibrillary tangles composed of tau protein. AD pharmacotherapy aims to manage cognitive symptoms, delay disease progression, and treat behavioral symptoms. The treatment is primarily symptomatic and palliative, with no definitive disease-modifying therapy available. Cholinesterase inhibitors, including donepezil (Aricept), rivastigmine (Exelon), and galantamine (Razadyne), are...
Alzheimer's Disease: Overview
Alzheimer's Disease (AD) is a continually advancing neurodegenerative disorder, distinguished by escalating memory loss, cognitive dysfunction, and dementia. The disease unfolds in three stages: preclinical, mild cognitive impairment (MCI), and dementia. Its onset is insidious, and the progression gradual, with the cause not well explained by other disorders.
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
The clinical diagnosis of AD hinges on the presence of memory and other cognitive impairments. Biomarkers, such as changes in Aβ and tau...
Alzheimer Disease ll: Pathophysiology
Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and microglia. Abnormal...
Alzheimer Disease l: Introduction
Alzheimer disease is a chronic, progressive, and irreversible neurodegenerative disorder and the most common cause of dementia in older adults. It leads to gradual neuronal loss, causing cognitive decline, behavioral changes, and loss of functional independence.Risk Factors and EtiologyThe disease is multifactorial. Age is the strongest risk factor, with prevalence doubling every 5 years after age 65. Genetic factors include mutations in genes such as APP, PSEN1, and PSEN2, which are associated...
Dementia l: Introduction
Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...
