Female Pattern Hair Loss and Negative Psychological Impact: Possible Role of Brain-derived Neurotrophic Factor (BDNF).

INTRODUCTION: Female Pattern Hair Loss (FPHL) is considered the most common type of hair loss in females. Women with FPHL may suffer from psychological distress and defective social functioning. Patients with psychiatric and neurodegenerative disorders almost have a deficient brain and blood brain-derived neurotrophic factor levels (BDNF). This serum BDNF level may act as a diagnostic marker for negative psychological impact in FPHL patients. OBJECTIVES: Evaluate the levels of serum BDNF in patients with FPHL and correlate its level to the severity of alopecia and the degree of psychological impact. METHODS: Forty-six female patients with FPHL and 41 healthy age-matched female volunteers as a control were included in the study. Patients filled out a Dermatology Life Quality Index questionnaire. Both patients and controls filled Beck Depression Inventory, Beck Anxiety Inventory, and Perceived Stress Scale (PSS) questionnaires. Serum levels of BDNF were measured for all the participants using the ELISA technique. RESULTS: Patients with FPHL had significantly lower levels of BDNF and significantly higher Beck depression inventory score and PSS questionnaire scores. There is a significant negative correlation between serum levels of BDNF and Beck Depression Inventory, Beck Anxiety Inventory, and PSS questionnaire scores. CONCLUSIONS: Patients with FPHL are at a high risk to develop chronic stress and depression. The serum level of BDNF is a good predictor for the assessment of chronic stress and depression in FPHL patients.

Search for a two-input model for future investigations of 'synaptic tagging' in freely moving animals in vivo.

Processes of "synaptic tagging" guarantee synaptic input specificity after the induction of a protein synthesis-dependent late long-term potentiation (late-LTP). Distinct high-frequency stimulation can set a transient "synaptic tag" at the activated synapses, which captures plasticity-related proteins (PRPs) synthesized synapse-non-specifically in dendritic branches/compartments or the somata. Thus, only those synapses, which expressed a "tag", are also able to express late-LTP. Additionally, it was shown that the synthesis of PRPs is triggered by heterosynaptic, non-glutamatergic requirements during LTP-induction in tissue from adult animals. All these experiments were performed in hippocampal slices in vitro so far. Two questions now arise: first, is it possible to describe processes of 'synaptic tagging' in the intact, freely moving animal and second, is the stimulation of glutamatergic inputs sufficient to induce 'tagging' or is the co-activation of a modulatory-heterosynaptic input, also required for the process? We have first developed a technique, which allows us now to induce distinct forms of LTP at the ipsilateral CA1 site by specifically stimulating glutamatergic hippocampal structures at the contralateral site in the intact, freely moving rat. Thus, the used stimulation protocol allowed us to activate two separate synaptic inputs to the same neuronal stimulation, a pre-requisite for tagging-experiments to be investigated in vivo.

Functional inactivation of a fraction of excitatory synapses in mice deficient for the active zone protein bassoon.

Mutant mice lacking the central region of the presynaptic active zone protein Bassoon were generated to establish the role of this protein in the assembly and function of active zones as sites of synaptic vesicle docking and fusion. Our data show that the loss of Bassoon causes a reduction in normal synaptic transmission, which can be attributed to the inactivation of a significant fraction of glutamatergic synapses. At these synapses, vesicles are clustered and docked in normal numbers but are unable to fuse. Phenotypically, the loss of Bassoon causes spontaneous epileptic seizures. These data show that Bassoon is not essential for synapse formation but plays an essential role in the regulated neurotransmitter release from a subset of glutamatergic synapses.