Current and Novel Biomarkers for Alzheimer's disease

Sindhu Ramesh#; Manoj Govindarajulu#; Ellery Jones; Stella Knowlton; Lily Weeks; Vishnu Suppiramaniam; Timothy Moore; Muralikrishnan Dhanasekaran*

The rapid increase in the incidence of Alzheimer's disease (AD) in the approaching future prompts a need for an easy, efficient and precise diagnosis of the disease at its initial stages to halt or delay the disease progression. Conventional testing includes measuring amyloid beta and tau levels in the cerebrospinal fluid (CSF) aided by imaging techniques like positron emission tomography (PET) and magnetic resonance imaging (MRI).

Global Health Impact of Major Classes of "Designer Drugs": Structural, Pharmacological and Toxicological Overview

Mohammed Almaghrabi; Mohammed Majrashi; Darshini Desai; Ayaka Fujihashi; Jack Deruiter; Randall Clark C; Muralikrishnan Dhanasekaran*

Different botanical derived or synthetic addictive substances have been "misused" and/or "abused" for centuries around the world. To overcome the abuse by these substances, strict legal laws were constituted globally. However, novel and drugs with chemical structures similar to illegal psychoactive drugs substances (with a slight structural change) were manufactured in undercover laboratories to have the same or augmented psychostimulatory effects. Currently, the major classes of designer drugs are piperazines, cathinones, synthetic cannabinoids, synthetic opioids, tryptamines, and phenethylamines.

Mitochondrial dysfunction and the role of Mitophagy in Alzheimer's Disease

Sindhu Ramesh#; Manoj Govindarajulu#; Ellery Jones; Vishnu Suppiramaniam; Timothy Moore; Muralikrishnan Dhanasekaran*

Mitochondrial dysfunction and alteration in energy regulation occurs prior to the disease-defining amyloid beta peptide (Aβ) and Tau pathologies in the pathogenesis of Alzheimer's disease (AD). Dysfunctional Mitophagy, the process of removal of defective mitochondria through a complex and integrated cellular network is dysfunctional in AD. Mitophagy complements to synaptic dysfunction by prompting Aβ and Tau accumulation due to increasing oxidative stress and cellular energy insufficiencies leading to cognitive deficits.

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