Immunotherapy for Alzheimer Disease

Rosenberg, Roger N.

doi:10.1001/archneur.62.10.1506

Cited by 8 publications

(3 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Current AD therapy serves only to reduce the degree of impairment and improve the quality of lives of patients. But the disease cannot be prevented or cured [13,14,124,125] . Th e demonstration of active adult neurogenesis has since opened possibilities of repairing the mature CNS after degenerative neurological diseases like AD.…”

Section: Clinical Signifi Cance and Future Directionsmentioning

confidence: 99%

Nerve Growth Factor, Neural Stem Cells and Alzheimer’s Disease

2006

View full text Add to dashboard Cite

The protein family of the neurotrophins (NTs) comprises structurally and functionally related molecules such as nerve growth factor (NGF) which influences the proliferation, differentiation, survival and death of neuronal cells. In addition to their established functions for cell survival, NTs also mediate higher brain activities such as learning and memory. Changes in NT expression levels have thus been implicated in neurological diseases such as Alzheimer’s disease (AD), an age-related neurodegenerative disorder that is characterized by progressive loss of memory and deterioration of higher cognitive functions. The present review provides an overview of the functional role of NGF in neural stem cells and AD while pointing to a potential application of this peptide for the treatment of AD.

show abstract

Section: Clinical Signifi Cance and Future Directionsmentioning

confidence: 99%

Nerve Growth Factor, Neural Stem Cells and Alzheimer’s Disease

2006

View full text Add to dashboard Cite

show abstract

“…However, a first clinical trial has been abandoned due to the development of meningoencephalitis in some cases. The treatment of AD with Aβ vaccines remains yet a controversy [145][146][147][148]. Another promising approach is the application of NGF as a potential remedy for the treatment of AD.…”

Section: Resultsmentioning

confidence: 99%

Alzheimers Disease - An Interactive Perspective

Heese¹,

Akatsu

2006

CAR

View full text Add to dashboard Cite

Alzheimer's disease (AD) is an age-related neurodegenerative disorder that is characterized by a progressive loss in memory and deterioration of the higher cognitive functions. The brain of an individual with AD exhibits extracellular senile plaques of aggregated amyloid-beta-peptide (Abeta), intracellular neurofibrillary tangles (NFTs) that consist of hyperphosphorylated tau protein (P-tau) and a profound loss of basal forebrain cholinergic neurons that innervate the hippocampus and the neocortex. Recent data obtained via genomics, proteomics and molecular genetics, have gleaned new information with regard to the physiological and pathophysiological functions of the amyloid precursor protein (APP) and its cleavage product Abeta. This review glances over several aspects that may play a major role in the pathogenesis of AD providing an insight into APP's and Abeta's interplay with other cellular systems.

show abstract

“…Pre-clinical studies have shown some efficacy of vaccines and active immunotherapies against Aβ and p-Tau, but the translation to humans proved ineffective and with serious safety issues (Song et al, 2020). Among others, a vaccine against Aβ1-42 (Elan Pharmaceuticals, CA, USA) could remove amyloid plaques and improve perceptive function in transgenic animal models and AD patients (Janus et al, 2000;Vellas et al, 2009), but the clinical trial of the Aβ1-42 vaccine was suspended because of severe side effects like acute meningoencephalitis and cerebral hemorrhage (Rosenberg, 2005).…”

Section: Introductionmentioning

confidence: 99%

An Aβ3‑10‑KLH vaccine decreases Aβ plaques and astrocytes and microglia activation in the brain of APP/PS1 transgenic mice

Wang

Zhou

et al. 2022

Acta Neurobiol. Exp.

View full text Add to dashboard Cite

This study aimed to investigate β-amyloid peptide (Aβ) plaques and changes of astroglia and microglia in mice with Alzheimer's disease (AD). In this study, 18 transgenic mice with amyloid precursor protein (APP) /presenilin-1 (PS1) were randomized into the Aβ3-10-KLH vaccine, Aβ1-42 vaccine, and phosphate-buffered saline (PBS) groups. The mice were injected at different time points. The Morris water maze test was used to identify the spatial learning and memory abilities of the mice. Immunohistochemistry was done to examine the Aβ, glial fibrillary acidic protein, and transmembrane protein 119 (TMEM119). Correspondingly, enzyme-linked immunosorbent assay (ELISA) was done to measure interleukin (IL) -1β and tumor necrosis factor (TNF) -α in the brain of transgenic mice. The Morris water maze results showed that both the Aβ3-10-KLH vaccine and the Aβ1-42 peptide vaccine could improve the cognitive function of APP/PS1 transgenic mice significantly. Aβ3-10-KLH and Aβ1-42 inoculations reduced Aβ load and suppressed astrocytes and microglia proliferation in the cortex compared with the PBS group. While there was no significant difference between the two groups, Aβ3-10-KLH and Aβ1-42 vaccines decreased the brain levels of IL-1β and TNF-α as compared with the PBS group, but without difference between the two vaccines. In conclusion, early immunotherapy with an Aβ vaccine reduces the activation of glial cells and deposition of Aβ plaque in the brain of transgenic mice.

show abstract

Immunotherapy for Alzheimer Disease

Cited by 8 publications

References 14 publications

Nerve Growth Factor, Neural Stem Cells and Alzheimer’s Disease

Nerve Growth Factor, Neural Stem Cells and Alzheimer’s Disease

Alzheimers Disease - An Interactive Perspective

An Aβ3‑10‑KLH vaccine decreases Aβ plaques and astrocytes and microglia activation in the brain of APP/PS1 transgenic mice

Contact Info

Product

Resources

About