scholarly journals Alzheimer’s-Like Pathology at the Crossroads of HIV-Associated Neurological Disorders

Vaccines ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 930
Author(s):  
Divya T. Chemparthy ◽  
Muthukumar Kannan ◽  
Lila Gordon ◽  
Shilpa Buch ◽  
Susmita Sil

Despite the widespread success of combined antiretroviral therapy (cART) in suppressing viremia, the prevalence of human immunodeficiency virus (HIV)-associated neurological disorders (HAND) and associated comorbidities such as Alzheimer’s disease (AD)-like symptomatology is higher among people living with HIV. The pathophysiology of observed deficits in HAND is well understood. However, it has been suggested that it is exacerbated by aging. Epidemiological studies have suggested comparable concentrations of the toxic amyloid protein, amyloid-β42 (Aβ42), in the cerebrospinal fluid (CSF) of HAND patients and in the brains of patients with dementia of the Alzheimer’s type. Apart from abnormal amyloid-β (Aβ) metabolism in AD, a better understanding of the role of similar pathophysiologic processes in HAND could be of substantial value. The pathogenesis of HAND involves either the direct effects of the virus or the effect of viral proteins, such as Tat, Gp120, or Nef, as well as the effects of antiretrovirals on amyloid metabolism and tauopathy, leading, in turn, to synaptodendritic alterations and neuroinflammatory milieu in the brain. Additionally, there is a lack of knowledge regarding the causative or bystander role of Alzheimer’s-like pathology in HAND, which is a barrier to the development of therapeutics for HAND. This review attempts to highlight the cause–effect relationship of Alzheimer’s-like pathology with HAND, attempting to dissect the role of HIV-1, HIV viral proteins, and antiretrovirals in patient samples, animal models, and cell culture model systems. Biomarkers associated with Alzheimer’s-like pathology can serve as a tool to assess the neuronal injury in the brain and the associated cognitive deficits. Understanding the factors contributing to the AD-like pathology associated with HAND could set the stage for the future development of therapeutics aimed at abrogating the disease process.

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Zahra Bagheri ◽  
Pegah Noorshargh ◽  
Zahra Shahsavar ◽  
Peyman Jafari

Abstract Background Recently, extensive research has been reported the higher rate of depression and anxiety among people living with HIV/AIDS (PLWHAs) as compared to the general population. However, no single study has been carried out to investigate whether this disparity is a real difference or it happens due to lack of measurement invariance. This study aims to assess the measurement invariance of the Beck Anxiety Inventory (BAI) and 10-item Centre for Epidemiological Studies Depression Scale (CESD-10) questionnaires across PLWHAs and healthy individuals. Methods One hundred and fifty PLWHAs and 500 healthy individuals filled out the Persian version of the BAI and CESD-10 questionnaires. Multi-group multiple-indicators multiple-causes model (MG-MIMIC) was used to assess measurement invariance across PLWHAs and healthy people. Results Our findings revealed that PLWHAs and healthy individuals perceived the meaning of all the items in the BAI and CESD-10 questionnaires similarly. In addition, although depression scores were significantly higher in PLWHAs as opposed to the healthy individuals, no significant difference was observed in anxiety scores of these two groups. Conclusions The current study suggests that the BAI and CESD-10 are invariant measures across PLWHAs and healthy people which can be used for meaningful cross-group comparison. Therefore, in comparison to healthy individuals, higher depression score of PLWHAs is a real difference. It is highly recommended that health professionals develop therapeutic interventions and psychological supports to promote the mental health of PLWHAs which alleviate their depressive symptoms.


2021 ◽  
Author(s):  
Koharu Loulou Chayama ◽  
Jenna Valleriani ◽  
Cara Ng ◽  
Rebecca Haines‐Saah ◽  
Rielle Capler ◽  
...  

2013 ◽  
Vol 69 (1) ◽  
Author(s):  
S. Cobbing ◽  
V. Chetty ◽  
J. Hanass-Hancock ◽  
J. Jelsma ◽  
H. Myezwa ◽  
...  

Despite increased access to highly active anti-retroviral therapy (HAART) in South Africa, there remains a high risk of people living with HIV (PLHIV) developing a wide range of disabilities. Physiotherapists are trained to rehabilitate individuals with the disabilities related to HIV. Not only can South African physiotherapists play a significant role in improving the lives of PLHIV, but by responding proactively to the HIV epidemic they can reinforce the relevance and value of the profession in this country at a time when many newly qualified therapists are unable to secure employment. This paper offers recommendations that may help to fuel this response. These ideas include enhancing HIV curricula at a tertiary level, designing and attending continuing education courses on HIV and researching Southern African rehabilitation interventions for HIV at all levels of practice. furthermore, it is vital that physiotherapists are at the forefront of directing multi-disciplinary responses to the rehabilitation of PLHIV in order to influence stakeholders who are responsible for health policy formulation. it is hoped that this paper stimulates discussion and further ideas amongst physiotherapists and other health professionals in order to improve the quality and access to care available to PLHIV in South Africa.


Author(s):  
Ravi Ranjan Kumar ◽  
Lovekesh Singh ◽  
Amandeep Thakur ◽  
Shamsher Singh ◽  
Bhupinder Kumar

Background: Vitamins are the micronutrients required for boosting the immune system and managing any future infection. Vitamins are involved in neurogenesis, a defense mechanism working in neurons, metabolic reactions, neuronal survival, and neuronal transmission. Their deficiency leads to abnormal functions in the brain like oxidative stress, mitochondrial dysfunction, accumulation of proteins (synuclein, Aβ plaques), neurodegeneration, and excitotoxicity. Methods: In this review, we have compiled various reports collected from PubMed, Scholar Google, Research gate, and Science direct. The findings were evaluated, compiled, and represented in this manuscript. Conclusion: The deficiency of vitamins in the body causes various neurological disorders like Alzheimer’s disease, Parkinson’s disease, Huntington's disease, and depression. We have discussed the role of vitamins in neurological disorders and the normal human body. Depression is linked to a deficiency of vitamin-C and vitamin B. In the case of Alzheimer’s disease, there is a lack of vitamin-B1, B12, and vitamin-A, which results in Aβ-plaques. Similarly, in Parkinson’s disease, vitamin-D deficiency leads to a decrease in the level of dopamine, and imbalance in vitamin D leads to accumulation of synuclein. In MS, Vitamin-C and Vitamin-D deficiency causes demyelination of neurons. In Huntington's disease, vitamin- C deficiency decreases the antioxidant level, enhances oxidative stress, and disrupts the glucose cycle. Vitamin B5 deficiency in Huntington's disease disrupts the synthesis of acetylcholine and hormones in the brain.


2016 ◽  
Vol 27 (4) ◽  
pp. 449-455 ◽  
Author(s):  
Ghulam Abbas ◽  
Wajahat Mahmood ◽  
Nurul Kabir

AbstractDespite their possible causative role, targeting amyloidosis, tau phosphorylation, acetylcholine esterase, glutamate, oxidative stress and mitochondrial metabolism have not yet led to the development of drugs to cure Alzheimer’s disease (AD). Recent preclinical and clinical reports exhibit a surge in interest in the role of GABAergic neurotransmission in the pathogenesis of AD. The interaction among GABAergic signaling, amyloid-β and acetylcholine is shown to affect the homeostasis between excitation (glutamate) and inhibition (GABA) in the brain. As a consequence, over-excitation leads to neurodegeneration (excitotoxicity) and impairment in the higher level functions. Previously, the glutamate arm of this balance received the most attention. Recent literature suggests that over-excitation is primarily mediated by dysfunctional GABA signaling and can possibly be restored by rectifying anomalous metabolism observed in the GABAergic neurons during AD. Additionally, neurogenesis and synaptogenesis have also been linked with GABAergic signaling. This association may provide a basis for the needed repair mechanism. Furthermore, several preclinical interventional studies revealed that targeting various GABA receptor subtypes holds potential in overcoming the memory deficits associated with AD. In conclusion, the recent scientific literature suggests that GABAergic signaling presents itself as a promising target for anti-AD drug development.


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