Alzheimer’s Disease (AD), a progressive and debilitating condition, is reported to be the most common type of dementia, with at least 55 million people believed to be currently affected. Many causation hypotheses of AD exist, yet the intriguing link between viral infection and its possible contribution to the known etiology of AD has become an attractive focal point of research for the field and a challenging study task. In this review, we will explore the historical perspective and milestones that led the field to investigate the viral connection to AD. Specifically, several viruses such as Herpes Simplex Virus 1 (HSV-1), Zika virus (ZIKV), and severe cute respiratory syndrome coronavirus 2 (SARS-CoV-2), along with several others mentioned, include the various viruses presently considered within the field. We delve into the strong evidence implicating these viruses in the development of AD such as the lytic replication and axonal transport of HSV-1, the various mechanisms of ZIKV neurotropism through the human protein Musashi-1 (MSI1), and the spread of SARS-CoV-2 through the transfer of the virus through the BBB endothelial cells to glial cells and then to neurons via transsynaptic transfer. We will also explore beyond these mere associations by carefully analyzing the potential mechanisms by which these viruses may contribute to AD pathology. This includes but is not limited to direct neuronal infections, the dysregulation of immune responses, and the impact on protein processing (Aβ42 and hyperphosphorylated tau). Controversies and challenges of the virus–AD relationship emerge as we tease out these potential mechanisms. Looking forward, we emphasize future directions, such as distinct questions and proposed experimentations to explore, that the field should take to tackle the remaining unanswered questions and the glaring research gaps that persist. Overall, this review aims to provide a comprehensive survey of the past, present, and future of the potential link between viral infections and their association with AD development while encouraging further discussion.

Chronic mercury poisoning from cosmetics is often misdiagnosed and mistreated due to atypical clinical presentations and high industrial standards and quality control of cosmetic products. Here we present a case of a 45-year-old female with a four-month history of progressive weakness, atrophy, insomnia, mood swings, chorea-like movement, extremity pain and hyperalgesia. The routine workup for neuropathy and myopathy such as CK, EMG were unremarkable. However heavy metal screen revealed significantly elevated mercury levels. Afterwards, we found it was caused by daily-use whitening cosmetics through the hair segmented toxicant analysis to trace the dynamics changing of mercury concentration in the body. After the removal of the patient from the source of exposure, and chelation therapy, her symptoms had gradually improved. When patients have unexplained behavioral changes, cognitive decline, sleep disturbance, fatigue, pain, and other unspecific manifestations, the possibility of mercury poisoning should be considered, blood mercury and urine mercury should be detected, and the source of exposure should be investigated and timely treatment should be given.

HIV-sensory neuropathy (HIV-SN) is a debilitating complication in HIV patients with or without anti-retroviral treatment (ART). Common symptoms of HIV-SN include pain, decreased sensation, paresthesias, and dysesthesias in a symmetric stocking-glove distribution. While HIV-1 protein such as gp120 is implicated in HIV-SN (e.g. impaired large-diameter fiber), ART itself was recently shown to contribute to HIV-SN in HIV patients and impair thin fiber. Multiple host mechanisms may play roles during the pathogenesis of HIV-SN, including neuron-glia interactions in the spinal dorsal horn (SDH), inflammation, mitochondrial dysfunction and endoplasmic reticulum stress. Concurrent infections, such as tuberculosis, also carry a higher likelihood of HIV-SN as well as environmental or genetic predisposition. Pro-inflammatory cytokines such as IL-1, IL2 receptor-alpha, and tumor necrosis factor (TNF) along with abnormal lactate levels have been identified as potential players within the complex pathophysiology of this condition. In this paper, we review the pathophysiology of HIV neuropathy, focusing on the various treatment options available or under investigation. Although several treatment options are available e.g., the capsaicin patch and spinal cord stimulation, symptomatic control of HIV-SN are often challenging. Alternative approaches such as self-hypnosis, resistance exercise, cannabinoids, and acupuncture have all shown promising results, but need further investigation.

Some of the reported neurological manifestations of COVID-19 are encephalopathy, headache, ischemic, hemorrhagic stroke, Miller Fisher syndrome, cranial neuropathies, and Guillain-Barre syndrome. We report a case of a 75-year-old COVID-19 patient with life-threatening intracranial hemorrhage. The initial labs on admission showed D-dimer of 1.04 µg/mL, which increased to 3.74 µg/mL the next day, PT/INR of 13.7 seconds/1.2, aPTT of 22 seconds, fibrinogen of 386 mg/dL, WBC of 9.71 K/µL, Hgb of 14.1 g/dL, platelet of 315 x 10³/µL, LDH of 965 U/L, and CRP of 35.2 mg/dL. In addition to aspirin and Plavix (clopidogrel), the patient was started on a therapeutic dose of enoxaparin due to elevated D-dimer. A few days later, the patient had a change in the neurological examination. The CT of the head without contrast revealed a left-sided acute subdural hematoma, causing left to right midline shift, a large left temporal intraparenchymal, and subarachnoid hemorrhage with transtentorial herniation, leading to death. This case illustrates a combination of factors including hypertension, triple therapy (aspirin, clopidogrel, and enoxaparin), and underlying coagulopathy due to COVID-19, which contributed to the life-threatening intracranial hemorrhage in this patient. Therefore, this raises a concern about the safety of starting these patients preemptively on a therapeutic dose of anticoagulation.