However, the recent failure of drugs targeting tau deposits suggests a lack of accurate understanding of the complex pathophysiology of AD. Attention is now on therapies targeted at tau due to failures in β-amyloid clinical drug trials.

Studies reveal that the mutated, aberrantly folded, and hyperphosphorylated tau is less efficient in sustaining microtubule growth and function, resulting in the destabilization of the microtubule network-a hallmark of AD. Intracellular neurofibrillary tangles (NFTs) are commonly seen in AD brains and represent aberrantly folded and hyperphosphorylated isoforms of the microtubule-associated protein tau. However, the poor correlation of amyloid deposits with cognitive decline in the symptomatic phase of dementia may explain why drug targets to β-amyloid have not succeeded to date. Accumulated Aβ triggers neurodegeneration, resulting in clinical dementia that is characteristic of AD. The two prominent pathologic hallmarks of Alzheimer’s disease are (a) extracellular accumulation of β-amyloid deposits and (b) intracellular neurofibrillary tangles (NFT). It is believed that therapeutic intervention that could postpone the onset or progression of AD would dramatically reduce the number of cases over the next 50 years. Patients in the late–severe stage of AD will require comprehensive care owing to complete loss of memory and the disappearance of their sense of time and place. This loss results in gross atrophy of the affected regions, resulting in loss of memory, inability to learn new information, mood swings, executive dysfunction, and an inability to complete activities of daily living (ADLs). The underlying pathology is neuronal degeneration and loss of synapses in the hippocampus, cortex, and subcortical structures. Efforts to find a cure for AD have so far been disappointing, and the drugs currently available to treat the disease have limited effectiveness, especially if the disease is in its moderate–severe stage.

Being heterozygous or homozygous for the ApoE ε4 allele significantly increases the risk of developing Alzheimer’s. While the etiology is incompletely understood, genetic factors account for the 5 to 10% of cases that are familial Alzheimer’s, with the other 90 to 95% being sporadic. It is hoped that these medicinal plants can be used in drug discovery programs for identifying safe and efficacious small molecules for AD.Īlzheimer’s disease (AD) is one of the most significant global healthcare problems and is now the third leading cause of death in the United States. Conclusions-Medicinal plants have great potential as part of an overall program in the prevention and treatment of cognitive decline associated with AD.

PubMed Central, Scopus, and Google Scholar databases of articles were collected, and abstracts were reviewed for relevance to the subject matter. Methods-This article systematically reviews recent studies that have investigated the role of neuroprotective herbs and their bioactive compounds for dementia associated with Alzheimer’s disease and pre-Alzheimer’s disease. This article reviews a subset of herbs for their anti-inflammatory, antioxidant, and cognitive-enhancing effects. Indeed, several scientific studies have described the use of various medicinal plants and their principal phytochemicals for the treatment of AD. Medicinal plants and herbal remedies are now gaining more interest as complementary and alternative interventions and are a valuable source for developing drug candidates for AD. More than two hundred promising drug candidates have failed clinical trials in the past decade, suggesting that the disease and its causes may be highly complex. The pharmaceutical approaches developed to date do not alter disease progression. While the exact cause of AD is still unclear, recent studies point to lifestyle, diet, environmental, and genetic factors as contributors to disease progression. Background-Alzheimer’s disease (AD) is a multifactorial, progressive, neurodegenerative disease that is characterized by memory loss, personality changes, and a decline in cognitive function.

Teng to special treatment for amnesia