Autism Spectrum Disorder (ASD) is a complex neurodevelopmental condition characterized by challenges in communication, social interaction difficulties, and repetitive behaviors that can hinder a child’s development. The growing prevalence of autism necessitates early detection and effective intervention strategies. This review summarizes the current knowledge of early indicators of ASD, including brain development markers and behavioral signs visible in infants. It investigates diagnostic processes, emphasizing the importance of timely detection at 18 to 24 months using established screening tools. We discuss a variety of therapeutic approaches, including behavioral interventions, educational strategies such as music therapy, and technological advancements such as speech-generating devices. Furthermore, we investigate pharmacological options for treating associated symptoms, emphasizing the lack of targeted medications for core ASD symptoms. Finally, we present evidence highlighting the positive effects of early intervention on developmental outcomes, advocating for individualized treatment plans to enhance the well-being of children with ASD. This comprehensive overview aims to inform ongoing ASD research and clinical practices.

Amyotrophic Lateral Sclerosis (ALS) is a complex neurodegenerative disorder characterized by the death of motor neurons in the spinal cord and brain regions, leading to a reduced survival rate in patients. Nearly 20 gene mutations are associated with ALS, with SOD1, FUS, TARDBP, and C9orf72 mutations being more common. Ninety percent of ALS cases are related to sporadic ALS, while the remaining 10 % are associated with familial ALS. CRISPR/Cas9, a genome engineering technology known as clustered regularly interspaced short palindromic repeats/CRISPR-associated system 9, has the potential for gene editing and for studying the underlying mechanisms of ALS in mouse models. This technique enables neuroscientists to reverse mutations found in ALS mouse models, providing new hope for understanding the complexities of ALS. Additionally, this tool can create mutations to probe the functional changes of genetic diseases. Using CRISPR/Cas9 with an in vivo delivery method involving adeno-associated vectors, it is possible to silence mutations in the SOD1-linked ALS mouse model. Some limitations related to CRISPR/Cas9 have been discussed in previous studies and need to be addressed before clinical trials can proceed. In this review-based study, we summarise the latest research on CRISPR/Cas9 genome editing for ALS in mouse models and discuss its limitations and future prospects as well.

Traumatic brain injury (TBI) is an increasing widespread cause of disability and mortality, typically leading to dementia and memory impairment. This study aims to investigate the neuroprotective potential of Nigella sativa extract against TBI induced memory impairment in adult albino mice. Adult male mice were divided into four groups randomly: Control, Nigella sativa extract alone, TBI alone and TBI plus Nigella sativa extract. TBI induction was carried out in mice using a weight dropping method then Nigella sativa extract (10 mg/kg) was administered intraperitoneally for two weeks. Morris water maze and Y-maze tests were used to measure memory improvement ability and Western blot technique was used to analyse the neuroinflammatory and synaptic protein markers. Nigella sativa extract significantly decreased phosphorylated c-Jun N-terminal kinase (p-JNK), Tumor necrosis factor-alpha (TNF-α), and nuclear factor kappa B (NF-κB) proteins to reduce TBI-induced neuroinflammation accompanied by the restoration of both pre- and post-synaptic protein expression in adult mice model. Furthermore, Nigella sativa extract enhanced both short and long-term spatial memory against TBI in adult mice model. Nigella sativa extract abrogated neuroinflammation mediated memory impairment in TBI mice model. Further research is needed to determine Nigella sativa extract ingredients detail completely and to understand its mechanisms of neuroprotection in reducing memory impairments associated with traumatic brain injury and other neurodegenerative diseases.

Sumac (Rhus coriaria) is a spice and a medicinal plant that has been indicated to exert favorable effects in the management of different diseases, and it also possesses high anti-inflammatory and antioxidant properties. A plant known to be rich in bioactive molecules, including polyphenols, tannins, and flavonoids, sumac showed potent free radical scavenging activity. It thus may fight oxidative stress, which is recognized as the main cause of neurodegenerative ailments. In addition, recent investigations have also demonstrated during in vitro assays that Rhus coriaria might exert acetylcholinesterase inhibition activities, of interest in the context of therapeutic approaches for Alzheimer's disease (AD) associated with an increase of cholinergic neurotransmission supporting the cognitive processes. Furthermore, the sumac's neuroprotective activity may regulate amyloid-β (Aβ) aggregation, an important phenomenon in the AD diseased brain. Sumac may preserve neurons and synapses by blocking Aβ plaque production and neurotoxicity. That makes its anti-inflammatory activity additionally involve neuroprotective activity, largely because it reduces the pro-inflammatory cytokines level and restrains the microglial activation in the progression of AD. Given the multitarget activities, Rhus coriaria may be a potent natural candidate for preventing and treating AD. In vitro and in vivo studies are necessary to isolate its bioactive compounds, as well as preclinical and clinical studies for its effects on neurodegenerative and cognitive disorders. Dietary or medicative incorporation of sumac can supply an adjuvant choice for AD and its correlated pathogenicity.