Alzheimer's disease is distinguished by gradual changes in behavior because of the aggregation of β-amyloid and τ protein that blocks the signal transduction pathway. It is one of the major problems in the current scenario. It mainly occurs after the age of 60 and eventually leads to memory loss. Nonetheless medicinal plants have therapeutic potential to improve many diseases. Medicinal drugs with their phytoconstituents may offer therapeutic potential for improving the preventive treatment for Alzheimer's disease. Five synthetic drugs that have been approved by the FDA include Tacrine Rivastigmine Donepezil Galantamine and Memantine for the symptomatic treatment of Alzheimer's. In the search for effective anti-Alzheimer's drugs from a natural source we discovered marine resources as the origin of the therapeutic and nutritional compound. The methodology involves conducting a comprehensive literature survey. The database search methodology used in this review was the use of keywords which can be found in the article pertaining to Alzheimer’s disease. The significant articles focused on marine flora phytoconstituents such as acetylcholinesterase or butyrylcholinesterase inhibitors thus prompting a comprehensive review based on pertinent information. The review included descriptions of various studies revealing that numerous compounds derived from marine sources have demonstrated promising efficacy in the treatment of Alzheimer's disease. Many compounds that originated from marine sources showed good efficacy in treating Alzheimer’s disease. Acetylcholinesterase or butyrylcholinesterase inhibition was the main pharmacological mechanism that was reported for most of the molecules however few articles having alternative anti Alzheimer’s mechanisms have also been reported. This article highlights marine compounds derived from marine sources like algae fungi and sponges which can combat Alzheimer's disease.

Neuroleptic drug therapy used to manage psychotic disorders often induces hormonal disruptions that can impact patient health and treatment outcomes. This review explores the relationship between neuroleptic medications and the endocrine system highlighting current insights and clinical challenges. Antipsychotic drugs often elevate prolactin levels leading to hyperprolactinemia which manifests as galactorrhea amenorrhea and sexual dysfunction. These medications can also alter insulin and glucagon levels contributing to metabolic syndromes like type 2 diabetes and insulin resistance. Disruption of thyroid hormone homeostasis can result in hypothyroidism or hyperthyroidism exacerbating psychiatric symptoms. Moreover neuroleptic drugs affect growth hormone and adrenal function potentially causing weight gain and adrenal insufficiency. Understanding these hormonal side effects is crucial for developing treatment plans that mitigate adverse effects while optimizing psychiatric care. Despite advances in psychopharmacology challenges remain in predicting individual patient responses and managing long-term endocrine complications. Current research underscores the need for routine endocrine monitoring in patients on neuroleptic therapy and exploring adjunctive treatments to counteract these side effects. Future studies should focus on elucidating the molecular mechanisms underlying these hormonal disruptions and developing targeted interventions to improve patient outcomes. This review provides an overview of the hormonal side effects of neuroleptic drugs emphasizing the importance of interdisciplinary approaches in addressing the needs of patients with psychotic disorders.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline memory loss and functional impairment. Despite extensive research effective treatments remain elusive highlighting the need for innovative therapeutic approaches. This review article explores enzymatic targets and drug development strategies aimed at combating AD. Key enzymatic targets include beta-secretase (BACE1) gamma-secretase and tau protein kinases all of which play critical roles in the pathogenesis of AD. BACE1 and gamma-secretase are involved in the production of amyloid-beta (Aβ) peptides whose aggregation forms the hallmark amyloid plaques in AD brains. Inhibitors targeting these enzymes aim to reduce Aβ production and accumulation. Tau protein kinases such as glycogen synthase kinase-3 (GSK-3) and cyclin-dependent kinase 5 (CDK5) are implicated in tau hyperphosphorylation and subsequent neurofibrillary tangle formation. Modulating these kinases offers the potential for reducing tau pathology. The review further discusses various drug development strategies including small-molecule inhibitors monoclonal antibodies and gene therapy. Small molecule inhibitors such as BACE1 and gamma-secretase inhibitors have shown promise in preclinical studies but face challenges related to specificity and side effects. Monoclonal antibodies targeting Aβ and tau provide an alternative approach with several candidates currently undergoing clinical trials. Gene therapy represents a cutting-edge strategy aiming to correct or modulate disease-causing genetic mutations. In summary targeting enzymatic pathways involved in AD pathogenesis offers a promising avenue for drug development. While significant challenges remain ongoing research and clinical trials continue to advance our understanding and potential treatment options for this debilitating disease.

The Brain: A Systems Neuroscience Perspective is a comprehensive textbook designed for undergraduate students in neuroscience. It offers a detailed exploration of brain dynamics spatial navigation and the neuroscience of Alzheimer's disease with an emphasis on understanding complex concepts through simplified mathematical models. The objective is to provide a solid foundation for readers in systems neuroscience.

Key Topics

Fundamental Brain Dynamics: Covers the basics of brain organization neural systems and the role of differential equations in neuroscience (Chapters 1-3).

Spatial Navigation: Discusses the neural mechanisms underlying spatial navigation and the geometry of neural maps (Chapter 4).

Alzheimer’s Disease: Presents a simplified mathematical theory of Alzheimer’s dementia exploring its onset progression and potential interventions (Chapter 5).

Key Features

Accessible Approach: Minimizes mathematical complexity to make the subject approachable for readers with a basic understanding of differential equations.

Standalone Resource: Provides all essential knowledge on brain function making it a valuable tool for both coursework and self-study. Includes references for advanced readers.

Tardive dyskinesia (TD) is induced by antipsychotic drugs that have dopamine-antagonising properties. It frequently causes physical and mental anguish in individuals lowering their quality of life. Recent research on the aetiology and pathogenesis of TD indicates that genetic predisposition treatment options age sex and lifestyle factors are among the key risk factors contributing to the development of TD. Various genetic polymorphisms along with severe oxidative stress and other diseased conditions help to precipitate TD while on antipsychotic medications or other dopamine receptor blockers. Individuals diagnosed with schizophrenia are at a higher likelihood of developing TD. The current piece of literature aims to review the probable underlying mechanisms of TD explore its pathophysiology address the diagnostic challenges and present the available treatment options. This comprehensive analysis draws from a range of published peer-reviewed publications presenting the information in a clear and accessible manner.

Depression is one of the most challenging diseases for society to treat. It is a highly prevalent and disabling illness in the general population. Affective disorders are characterised by depressed mood diminished interest and pleasure feelings of guilt or poor self-worth sleep or food difficulties decreased energy and impaired attention. This manuscript will look at depression from a behavioural analytic perspective. The pathogenesis of major depressive disorder is poorly understood. Several lines of experimental and clinical evidence however show that the therapeutic effect of most antidepressant drugs is related to an increase in 5-HT-mediated neurotransmission. Alternative techniques however are employed to obtain this net effect. A better understanding of the neurological mechanism underpinning antidepressant drugs' delayed onset of action has resulted in the development of ways to accelerate antidepressant responses which are discussed further below. Many antidepressant medications on the market today are beneficial but they come with many downsides including unpleasant side effects potential interactions and a low response rate. Natural drugs on the other hand are extremely effective have a low risk and a limited amount of side effects which are covered briefly in this paper. Alternative modalities of administration have received a lot of attention in recent decades as a complement to approved prescription pharmaceuticals especially for people who cannot tolerate oral or parenteral methods. The most promising non-invasive systemic delivery techniques are transdermal and transbronchial administration and these are the focus of this research.

A review is presented as to the neurochemical basis of the straight runway task usually consisting of an acquisition phase followed by an extinction phase. During the acquisition of the appetitive runway task running speeds from the start box to the goal box progressively increase over trials and then decrease when the reward is withheld. Runway extinction is susceptible to lesions of the limbic system including the medial frontal cortex the hippocampus the septum the amygdala and the dorsomedial thalamus. When specific neurotransmitter systems are examined extinction was delayed when noradrenaline transmission was impeded perhaps involving noradrenergic projections to the hippocampus and neocortex. Extinction was likewise delayed after either facilitation or blocking of dopamine transmission a result implicating an inverted U-shaped function caused by dopamine’s role in behavioral activation or reward processes. Extinction was also delayed by indirect GABAA receptor agonists injected during acquisition explained by drug-induced disinhibitory tendencies. This simple paradigm may provide information about the effects of a physiological manipulation on both cognition and emotion.

This narrative review delves into the potential therapeutic implications of semaglutide a Glucagon-Like Peptide-1 (GLP-1) receptor agonist in the context of Substance Use Disorders (SUDs). By systematically exploring databases from 2011 to 2023 and incorporating foundational works from 2004 a total of 59 articles were identified as pertinent to the topic. Utilizing the SANRA scale for assessment the quality and relevance of these studies were rigorously evaluated. Preliminary findings indicate that semaglutide may play a pivotal role in modulating behaviors associated with SUDs potentially providing fresh perspectives on the neurobiological mechanisms underlying these disorders. While the precise pathways of action for semaglutide remain to be fully deciphered its recurrent mention in the literature underscores its emerging importance in the field of SUD research. As the understanding of semaglutide's influence expands it holds promise as a focal point in future studies warranting further in-depth exploration to ascertain its full therapeutic potential.