Somatostatin, Alzheimer's disease and cognition: An old story coming of age?

Laminar and cellular analyses of reduced somatostatin gene expression in the subgenual anterior cingulate cortex in major depression

“…This model is consistent with findings of reduced SST expression in other brain disorders, since the potential mechanistic events listed above occur in multiple contexts and are not specific to MDD. Indeed, reduced SST expression has been reported in schizophrenia (Morris et al, 2008), bipolar disorder (Konradi et al, 2004; Konradi et al, 2011), Alzheimer’s disease (Epelbaum et al, 2009; Gahete et al, 2010), as well as during normal aging of the human brain (Glorioso et al, 2011). See (Martel et al, 2012) for a comprehensive review of SST changes across brain disorders.…”

Aging, but not tau pathology, impacts olfactory performances and somatostatin systems in THY-Tau22 mice

“…The selective vulnerability of SOM cells in pathophysiological aging is well described in AD experimental models overexpressing human tau or APP (for review, Epelbaum et al, 2009), where hippocampal SOM interneurons loss is correlated to behavioral cognitive impairment (Andrews-Zwilling et al, 2010;Levenga et al, 2013;Perez-Cruz et al, 2011;Ramos et al, 2006) olfactory deficits are observed (Rey et al, 2011;Wesson et al, 2010a). Because postmortem and clinical studies led to the consensus that NFT are better neuropathologic correlates of AD clinical symptoms than Ab pathology based on progression and severity of cognitive impairment (Duyckaerts et al, 2009;Nelson et al, 2012) the impact of tau pathology on odor processing required cautious evaluation.…”

“…A consistent set of data relates the selective vulnerability of somatostatin (SOM) levels, a major brain inhibitory peptide to normal and pathophysiological aging (reviewed in Epelbaum et al, 2009;Stanley et al, 2012). In AD human cortex or cerebrospinal fluid samples as in experimental models, the decline of SOM levels is correlated with the progression of neuropathologic hallmarks (Ramos et al, 2006;Tan et al, 2010) and the extent of cognitive impairment (Andrews-Zwilling et al, 2010;Bierer et al, 1995;Grouselle et al, 1998;Perez-Cruz et al, 2011).…”

Somatostatin and Cognitive Function in Neurodegenerative Disorders

“…Taken together, the experimental data that have been accumulated during the past 40 years have proved the localization of specific sst subtypes in regions of the brain implicated in locomotor activity, sensory perception, learning and memory, and suggest that SST plays a substantial role in memory and cognition. In their recent review, Epelbaum et al concluded that SST deficit is a generalized marker for many brain disorders associated with cognitive impairments, and therefore relates to the pathophysiology of cognitive deficits in general rather than to the aetiology of a specific neuropathology [19]. There is general agreement that a low SST level or sst impairment can contribute to AD, but the results relating to the signficance of this system in the other three neurologic diseases are inconsistent.…”

“…However, the functional role and development of these pathways are still subjects of extensive examination. In a recent review, Epelbaum et al emphasized the role of the hippocampal somatostatinergic pathways in memory, cognition and emotions [19].…”