Brain cells of a laboratory mouse glowing with multicolor fluorescent proteins. Image courtesy of Harvard University, Livett-Weissman-Sanes-Lichtman
Early growth factor treatment may help prevent cell loss in Alzheimer’s disease
Brain-derived neurotrophic factor or BDNF has long been a target of interest among Alzheimer’s disease (AD) researchers and the Alzheimer’s community at large.
Four years ago, Mark Tuszynski, MD, PhD, professor of neurosciences at UC San Diego School of Medicine and director of the Center for Neural Repair and colleagues showed that a BDNF-based treatment measurably improved neural dysfunction in animal models of Alzheimer’s disease. The findings garnered international headlines.
Now there is new evidence that BDNF may be effective as a preventive measure for AD. 
In a paper, published yesterday in The Journal of Neuroscience, Tuszynski and colleagues follow up with evidence that early life BDNF treatment prevents neuronal loss in mutant mice genetically predisposed to early-onset familial Alzheimer’s disease.
Specifically, mice engineered to express APP, a protein strongly linked to AD development, received injections of the BDNF gene at two months of age and were examined five months later. The researchers found that BDNF-treated mice exhibited better behavior and brain function than untreated APP mutant mice and suffered significantly less neuron loss in the entorhinal cortex, a region of the brain that helps mediate learning and memory.
In addition, they noted that BDNF did not affect amyloid plaque accumulation, another major indicator of AD, suggesting that direct amyloid reduction is not necessary to achieving significant neuroprotective benefits in mutant amyloid models of AD.
“These findings strengthen the rationale for planning human clinical trials of BDNF therapy in AD,” said Tuszynski. “This is an effort that we are actively engaged in.” 
Tuszynski also noted that there is a possibility that BDNF therapy and anti-amyloid therapies for AD could be combined to yield better treatments than either treatment alone.

Brain cells of a laboratory mouse glowing with multicolor fluorescent proteins. Image courtesy of Harvard University, Livett-Weissman-Sanes-Lichtman

Early growth factor treatment may help prevent cell loss in Alzheimer’s disease

Brain-derived neurotrophic factor or BDNF has long been a target of interest among Alzheimer’s disease (AD) researchers and the Alzheimer’s community at large.

Four years ago, Mark Tuszynski, MD, PhD, professor of neurosciences at UC San Diego School of Medicine and director of the Center for Neural Repair and colleagues showed that a BDNF-based treatment measurably improved neural dysfunction in animal models of Alzheimer’s disease. The findings garnered international headlines.

Now there is new evidence that BDNF may be effective as a preventive measure for AD. 

In a paper, published yesterday in The Journal of Neuroscience, Tuszynski and colleagues follow up with evidence that early life BDNF treatment prevents neuronal loss in mutant mice genetically predisposed to early-onset familial Alzheimer’s disease.

Specifically, mice engineered to express APP, a protein strongly linked to AD development, received injections of the BDNF gene at two months of age and were examined five months later. The researchers found that BDNF-treated mice exhibited better behavior and brain function than untreated APP mutant mice and suffered significantly less neuron loss in the entorhinal cortex, a region of the brain that helps mediate learning and memory.

In addition, they noted that BDNF did not affect amyloid plaque accumulation, another major indicator of AD, suggesting that direct amyloid reduction is not necessary to achieving significant neuroprotective benefits in mutant amyloid models of AD.

“These findings strengthen the rationale for planning human clinical trials of BDNF therapy in AD,” said Tuszynski. “This is an effort that we are actively engaged in.” 

Tuszynski also noted that there is a possibility that BDNF therapy and anti-amyloid therapies for AD could be combined to yield better treatments than either treatment alone.

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