Modifiable factors that alter the size of the hippocampus with ageing

Abstract

The hippocampus is particularly vulnerable to the neurotoxic effects of obesity, diabetes mellitus, hypertension, hypoxic brain injury, obstructive sleep apnoea, bipolar disorder, clinical depression and head trauma. Patients with these conditions often have smaller hippocampi and experience a greater degree of cognitive decline than individuals without these comorbidities. Moreover, hippocampal atrophy is an established indicator for conversion from the normal ageing process to developing mild cognitive impairment and dementia. As such, an important aim is to ascertain which modifiable factors can have a positive effect on the size of the hippocampus throughout life. Observational studies and preliminary clinical trials have raised the possibility that physical exercise, cognitive stimulation and treatment of general medical conditions can reverse age-related atrophy in the hippocampus, or even expand its size. An emerging concept--the dynamic polygon hypothesis--suggests that treatment of modifiable risk factors can increase the volume or prevent atrophy of the hippocampus. According to this hypothesis, a multidisciplinary approach, which involves strategies to both reduce neurotoxicity and increase neurogenesis, is likely to be successful in delaying the onset of cognitive impairment with ageing. Further research on the constellation of interventions that could be most effective is needed before recommendations can be made for implementing preventive and therapeutic strategies.

Obesity and psychiatric disorders: Commonalities in dysregulated biological pathways and their implications for treatment

“…Investigations into structural brain changes has largely confirmed that obese and overweight individuals have a smaller hippocampal size compared to healthy individuals (Fotuhi et al, 2012, Mueller et al, 2012, Raji et al, 2010, Taki et al, 2008. A higher mid-life BMI also increases the rate of hippocampal atrophy in late life (Jagust et al, 2005, Taki et al, 2008.…”

Clinical Semiology and Neuroradiologic Correlates of Acute Hypernatremic Osmotic Challenge in Adults: A Literature Review

“…The high hippocampal involvement may be related to its high vulnerability to the neurotoxic effects of osmotic derangements 49 and systemic stresses in general. 50,51 In reviewed cases, contrast enhancement associated with ODS lesions was reported in 1 patient, 23 which has also been reported in some cases of hyponatremia. 52 Although inconsistently found, contrast enhancement is in agreement with the pathophysiologic changes observed in experimental models of ODS, in which BBB disruption occurs secondary to osmotic stress and is thought to be one of the leading factors in pathogenesis of ODS.…”

Neurobiological underpinnings of bipolar disorder focusing on findings of diffusion tensor imaging: a systematic review

“…78 Of note, WM is particularly vulnerable to the inflammatory neurotoxic Diffusion tensor imaging in BD effects of BD. 79 The cognitive decline that occurs over the course of the disease seems to be associated, at least in part, with vulnerability to the toxic effects of inflammation. 79 Additionally, immune disturbances have been linked to BD and symptom severity, mood episodes, staging, effect of medications, metabolic disturbances, neurotrophin alterations, and increased frequency of comorbid autoimmune and allergic disorders.…”

“…79 The cognitive decline that occurs over the course of the disease seems to be associated, at least in part, with vulnerability to the toxic effects of inflammation. 79 Additionally, immune disturbances have been linked to BD and symptom severity, mood episodes, staging, effect of medications, metabolic disturbances, neurotrophin alterations, and increased frequency of comorbid autoimmune and allergic disorders. 80 In this context, DTI findings could provide a better understanding of the neurobiological underpinnings of pathophysiology in BD.…”