127 Drevets et al128 recently reported reductions in 5-HT1A binding of [11C]WAY100635 to mcsiotemporal and brainstem raphe

areas in familial mood disorders including bipolar dépressives. Whether this finding is generalizable to selleck screening library nonfamilial forms of mood disorders and late-life depression is yet uncertain. The capability to selectively evaluate neurotransmitter binding sites in vivo will likely continue to be a valuable tool for determining the biological underpinnings of late-life depression and sources of Inhibitors,research,lifescience,medical treatment response variability among patients. Figure 2. Combined structural and functional imaging. The sagittal brain image (left) illustrates the distribution of 5-HT transporter binding sites imaged with positron emission tomography (PET) and [11C](+)-McN5652 (summed over 40 to 90 min postinjection). High-resolution … Alzheimer’s disease: breaking the disease barrier Alzheimer’s

disease (AD), the most common form of dementia, has enormous and growing public health significance. A disease of aging, the financial and social burdens of AD are compounded Inhibitors,research,lifescience,medical by recent and continued increases in the average life span.129,130 It has been estimated that the prevalence of AD will continue to climb at, a rapid rate, with an expected quadrupling of cases in the United States over the next, 50 years.130 Inhibitors,research,lifescience,medical Thus, the need for developing early diagnostic markers to complement new therapeutic approaches is more acute than ever before. Indeed, a modest goal of instituting treatment that could delay disease onset by just 2 years would profoundly impact these projections, Inhibitors,research,lifescience,medical resulting in 2 million fewer cases by 2050. Biological basis of Alzheimer’s disease Cell death and histopathological changes affecting a number of neuronal systems are considered to result in the development of the typical symptomatology of AD characterized by gross and progressive impairments of cognitive function. The histopathological features are intracellular neurofibrillary tangles formed from a hyperphosphorylated form of the microtubule-associatcd protein, tau, and extracellular Inhibitors,research,lifescience,medical deposits of a 40/42 amino acid peptide, Aβ (derived from amyloid

precursor protein PD184352 (CI-1040) [APP]), often in the form of senile or neuritic plaques. Plaques, tangles, and cell loss have a characteristic regional and temporal distribution in the AD brain, affecting entorhinal, hippocampal, and temporal cortical structures first and frontal and parietal cortices later in the disease process, while sparing primary sensory and primary motor areas.131 Indeed, this pathology is reflected in the characteristic regional pattern of blood flow and metabolic disturbances demonstrated by PET or SPECT imaging in early AD. Evidence from biochemical studies also indicates that certain subcortical stuctures, including the nucleus basalis of Meynert and the dorsal raphe are also affected early in the disease.