**6. Mood and communication disorders**

In addition to aging, neurodegenerative and psychiatric conditions, olfactory deficits including low OI appear as characteristic feature of mild to severe major

**103**

**7. Drugs**

*Neurological and Neuropsychiatric Disorders in Relation to Olfactory Dysfunction*

depression patients in comparison to normal controls [90]. Moreover,

Declined olfactory acuity and olfactory dysfunction are also evident in individuals suffering with post-traumatic stress disorder (PTSD) and in patients diagnosed with major depressive disorder (MDD). PTSD leads to decreased olfactory bulb volume, thereby leading to decreased olfactory acuity, additional olfactory deficits and dysfunction [35]. MDD indicates decline in both primary and secondary olfactory processing [84, 91]. MDD patients denote lower score for olfactory threshold, odor discrimination in 40-point smell identification test in comparison to normal controls At the same time, patients with olfactory dysfunction show clear symptoms of depression that become acute in comparative analysis

ASD adult patients show decline in odor identification ability [92]. Experimental evidence in two different mouse models of ASD indicates weaker and fewer synapses between olfactory sensory nerve terminals and olfactory bulb tufted cell layer; and weaker synapses between olfactory sensory nerve terminals and inhibitory periglomerular cells of the olfactory bulb [93]. Duplication of GABA receptor genes and deletion of TOP3B, topoisomerase involved in relaxation of supercoiled DNA contribute to autism susceptibility and have been assigned to gene families with specific contribution to neurodevelopmental disorders [94]. Out of 102 identified genes that contribute to ASD, most genes are expressed and enriched early in excitatory and

The regenerative ability of olfactory epithelium has made it an attractive target for exploring and evaluating therapeutic strategies to distinguish and treat drug induced olfactory disorders [96]. More than 86% of cancer patients of wide age range display smell and taste disorders that persist even after completion of chemotherapy for cancer [97]. However, not every therapeutic chemotherapy drugs has negative impact on olfactory acuity (personal communication). *Bacopa monnieri* extracts administration reverses bulbectomy induced neurochemical and histological alterations in mouse model of depression; cognition dysfunction is reversed through a mechanism that enhances synaptic plasticity related signaling, BDNF

The flavonoid Naringenin functions as antidepressant by restoring serotonin and noradrenaline levels in brain tissue [99]. In bulbectomized mice, two weeks of Naringenin treatment ameliorated depression like behavioral alterations, decreased

depressive disorders [81, 82]. As there is overlap in brain regions involved in AD, depression and olfactory processing, olfactory dysfunction could be the potential early biomarker of both AD and depressive disorders [83]. Similar to research studies using animal models that indicate a strong link between loss of olfaction and depressive behavior, a comparative analysis of age matched control individuals and patients diagnosed with depression showed loss of normal olfaction as marker of depression in humans [84]. Literature reviews of multiple research findings using specific parameters indicate a clear and consistent relation between depression and poor life quality in individuals from both clinical and community setting in age dependent manner [85]. Encoded olfactory stimuli activate emotional memory [86]; olfactory system and brain circuits participating in memory and cognition show a close anatomical link as well as frequent functional alteration in patients with depression [87–89]. Additional analysis clearly denotes a reciprocal relationship between olfaction and depression; patients with olfactory dysfunction show worsening depressive symptoms while olfactory performance is clearly reduced in

*DOI: http://dx.doi.org/10.5772/intechopen.93888*

of hyposmic to anosmic subjects [90].

inhibitory neuronal lineages and affect synapses [95].

transcription and protection of cholinergic systems [98].

#### *Neurological and Neuropsychiatric Disorders in Relation to Olfactory Dysfunction DOI: http://dx.doi.org/10.5772/intechopen.93888*

depressive disorders [81, 82]. As there is overlap in brain regions involved in AD, depression and olfactory processing, olfactory dysfunction could be the potential early biomarker of both AD and depressive disorders [83]. Similar to research studies using animal models that indicate a strong link between loss of olfaction and depressive behavior, a comparative analysis of age matched control individuals and patients diagnosed with depression showed loss of normal olfaction as marker of depression in humans [84]. Literature reviews of multiple research findings using specific parameters indicate a clear and consistent relation between depression and poor life quality in individuals from both clinical and community setting in age dependent manner [85]. Encoded olfactory stimuli activate emotional memory [86]; olfactory system and brain circuits participating in memory and cognition show a close anatomical link as well as frequent functional alteration in patients with depression [87–89]. Additional analysis clearly denotes a reciprocal relationship between olfaction and depression; patients with olfactory dysfunction show worsening depressive symptoms while olfactory performance is clearly reduced in depression patients in comparison to normal controls [90]. Moreover,

Declined olfactory acuity and olfactory dysfunction are also evident in individuals suffering with post-traumatic stress disorder (PTSD) and in patients diagnosed with major depressive disorder (MDD). PTSD leads to decreased olfactory bulb volume, thereby leading to decreased olfactory acuity, additional olfactory deficits and dysfunction [35]. MDD indicates decline in both primary and secondary olfactory processing [84, 91]. MDD patients denote lower score for olfactory threshold, odor discrimination in 40-point smell identification test in comparison to normal controls At the same time, patients with olfactory dysfunction show clear symptoms of depression that become acute in comparative analysis of hyposmic to anosmic subjects [90].

ASD adult patients show decline in odor identification ability [92]. Experimental evidence in two different mouse models of ASD indicates weaker and fewer synapses between olfactory sensory nerve terminals and olfactory bulb tufted cell layer; and weaker synapses between olfactory sensory nerve terminals and inhibitory periglomerular cells of the olfactory bulb [93]. Duplication of GABA receptor genes and deletion of TOP3B, topoisomerase involved in relaxation of supercoiled DNA contribute to autism susceptibility and have been assigned to gene families with specific contribution to neurodevelopmental disorders [94]. Out of 102 identified genes that contribute to ASD, most genes are expressed and enriched early in excitatory and inhibitory neuronal lineages and affect synapses [95].
