Of particular interest to those studying Alzheimer disease are reviews from Randy Buckner at Washington University, St. Louis, and Dominic Walsh and Dennis Selkoe at University College Dublin and Harvard Medical School, respectively.

Buckner contends that factors that lead to aging are not the same as those that lead to AD. In normal aging, loss of executive function, which can be distinguished from AD-related memory losses, is more common. “In advanced aging,” he writes, “frontal-striatal systems are preferentially vulnerable to white matter change, atrophy, and certain forms of neurotransmitter depletion.” In AD, however, the medial temporal lobe and cortical networks are primarily targeted, Buckner notes. He also reviews recent literature which suggests that reserve compensatory factors can influence how rapidly a person ages mentally. Cognitive reserve, he contends, can explain why, of two people with similar brain decline, one will be devastated while the other is seemingly unaffected.

Walsh and Selkoe assess the molecular basis for AD. Their review centers on the role played by amyloid-β (Aβ) peptides, particularly focusing on the recent evidence that has uncovered the toxic nature of Aβ. “Diverse lines of evidence now suggest that Aβ plays a central role in the pathogenesis of neuronal dysfunction in AD,” they write. Yet the Aβ cascade hypothesis remains controversial because there is no direct relationship between the number of amyloid plaques and the severity of the disease. Addressing this issue, the authors review findings that demonstrate soluble Aβ can perturb synaptic function, block long-term potentiation, and disrupt synaptic plasticity, memory, and learned behavior.

Other reviews include one on long-term potentiation and long-term depression by Robert Malenka and Mark Bear, a discussion of the role of translation in memory by Susumu Tonegawa and colleagues, and the role of the neocortex in memory consolidation by Alcino Silva and colleagues. The full citation list is included below.—Tom Fagan.

Reference:
Malenka RC, Bear MF. LTP and LTD: An Embarrassment of Riches. Neuron 2004 September 30;44:5-21. Abstract

Dan Y, Poo M-M. Spike Timing-Dependent Plasticity of Neural Circuits. Neuron 2004 September 30;44:23-30. Abstract

Davis RL. Olfactory Learning. Neuron 2004 September 30;44:31-48. Abstract

Bailey CH, Kandel ER, Si K. The Persistence of Long-Term Memory: A Molecular Approach to Self-Sustaining Changes in Learning-Induced Synaptic Growth. Neuron 2004 September 30;44: 49-57. Abstract

Kelleher III RJ, Govindarajan A, Tonegawa S. Translational Regulatory Mechanisms in Persistent Forms of Synaptic Plasticity. Neuron 2004 September 30;44:59-73. Abstract

Rodrigues SM, Schafe GE, LeDoux JE. Molecular Mechanisms Underlying Emotional Learning and Memory in the Lateral Amygdala. Neuron 2004 September 30;44:75-91. Abstract

Dudai Y, Eisenberg M. Rites of Passage of the Engram: Reconsolidation and the Lingering Consolidation Hypothesis. Neuron 2004 September 30;44:93-100. Abstract

Wiltgen BJ, Brown RAM, Talton LE, Silva AJ. New Circuits for Old Memories: The Role of the Neocortex in Consolidation. Neuron 2004 September 30;44:101-108. Abstract

Eichenbaum H. Hippocampus: Cognitive Processes and Neural Representations that Underlie Declarative Memory. Neuron 2004 September 30;44:109-120. Abstract

Walker MP, Stickgold R. Sleep-Dependent Learning and Memory Consolidation. Neuron 2004 September 30;44:121-133. Abstract

Vertes RP. Memory Consolidation in Sleep: Dream or Reality. Neuron 2004 September 30;44:135-148. Abstract

Schacter DL, Slotnick SD. The Cognitive Neuroscience of Memory Distortion. Neuron 2004 September 30;44:149-160. Abstract

Kelley AE. Memory and Addiction: Shared Neural Circuitry and Molecular Mechanisms. Neuron 2004 September 30;44:161-179. Abstract

Walsh DM, Selkoe DJ. Deciphering the Molecular Basis of Memory Failure in Alzheimer's Disease. Neuron 2004 September 30;44:Pages 181-193. Abstract

Buckner RL. Memory and Executive Function in Aging and AD: Multiple Factors that Cause Decline and Reserve Factors that Compensate. Neuron 2004 September 30;44:195-208. Abstract