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VIEWS & REVIEWS: Paul Coleman, Howard Federoff, and Roger Kurlan A focus on the synapse for neuroprotection in Alzheimer disease and other dementias Neurology 2004; 63: 1155-1162 [Abstract] [Full text] [PDF]

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Reply to Brenner

Roger Kurlan, MD, Paul Coleman, PhD, Howard Federoff, MD, PhD   (2 February 2005)

A focus on the synapse for neuroprotection in Alzheimer disease and other dementias

Steven R. Brenner   (2 February 2005)

Reply to Brenner 2 February 2005
Roger Kurlan, MD, University of Rochester Mt. Hope Professional Building, 1351 Mt. Hope Avenue, Suite 100, Rochester, NY 14620, Paul Coleman, PhD, Howard Federoff, MD, PhD Send Correspondence to journal: Re: Reply to Brenner roger_kurlan{at}urmc.rochester.edu Roger Kurlan, MD, et al.	We appreciate and agree with the comments by Dr. Brenner pointing out that astrocytes are a critical element when considering the function and maintenance of synapses and may be a potential target for experimental "synaptoprotective" therapies.
A focus on the synapse for neuroprotection in Alzheimer disease and other dementias 2 February 2005
Steven R. Brenner, St. Louis VA and St. Louis Univ. Neurology 61 North Tealwood, Saint Louis, MO 63141 Send Correspondence to journal: Re: A focus on the synapse for neuroprotection in Alzheimer disease and other dementias SBren20979{at}aol.com Steven R. Brenner	I read with interest the article by Coleman et al [1] with reference to synapse deterioration in AD. Preserving synaptic structure and function will probably be essential for successful treatment of AD. Astrocytes form an intimate relationship with synapses throughout the adult CNS, and have strong control over the number of synapses which form, are essential for postsynaptic function, and are necessary for synaptic stability and maintenance. [2] Astrocytic glia are involved in synaptic function, with stimulation of synaptogenesis and also maintenance of synaptic function with prevention of excessive glutamate leakage by enveloping synapses and also taking up excess glutamate which may leak out of the synaptic cleft. Few synapses form in the absence of glial cells and the few that form are functionally immature. [3] Astrocytes are intimately associated with the synapse, enwrapping many pre- and post- synaptic terminals [4] and reduce leakage of neurotransmitters such as glutamate from the synapse and also are active in taking up glutamate which may escape from the synapse. Astroyctes surround neurons, especially at the synaptic gap, where transmitters cross the synaptic cleft between one neuron’s axon and the next neuron's dendrite. They supply neurons with nutrients from blood vessels, absorb neurotransmitters when needed to help shut down neurons sending them and also communicate along networks using the same neurotransmitters neurons use, but are controlled by rising and falling concentrations of calcium ions. [5] Enhancing astrocytic maintenance of synapses may enhance synaptic preservation and arrest the development or progression of Alzheimer’s and related disorders where synaptic dysfunction and loss appears to be the rule. References 1. P Coleman, H Federoff, R Kurlan. A focus on the synapse for neuroprotectionin Alzheimer disease and other dementias. Neurology. 2004; 63: 1155-1162. 2. EM Ullian, KS. Christopherson, BA. Barres. Role for glia in synaptogenesis. Glia. 2004 47(3): 209-16. 3. EM Ullian, KS Sapperstein, KS Christopherson, BA Barres. Control of synapse number by Glia. Science. 2001. 291 (5504): 569-70. 4. E. Hansson, L Ronnback. Glial neuronal signaling in the central nervous system. FASEB J. 2003;17:341-348. 5. C. Krebs, K Huttmann, C Steinhauser. The forgotten brain emerges. Scientific American. 2004. 14; 5: 40-43.