Stress is frequently linked to or exacerbates a variety of illnesses, from psoriasis to digestive problems, possibly due to weakened immunity. Stress may play a role in both speeding the onset and exacerbating the course of Alzheimer's disease, according to new research.

What Effects Does Stress Have on the Body?

Stress is known to boost the synthesis and release of stress hormones such as corticosteroids (e.g. cortisol) as well as adrenalin by activating important brain areas such as the hypothalamic-pituitary-adrenal (HPA) axis.

Cortisol raises blood sugar levels and helps the brain to utilize insulin more efficiently, resulting in a rise in heart rate, blood pressure, and energy levels. It also suppresses normal immunological responses, digestive function, sexual performance, and other 'non-essential' activities at the same time. Stress has an influence not only on the body but also on the brain.

Long-term, recurrent, or chronic stress can harm a variety of physiological systems, resulting in anxiety, depression, insomnia, cardiovascular disease, digestive problems, and perhaps cognitive impairment, leading to early-stage dementia.

Alzheimer's Disease and Stress

Because studying and manipulating stress in humans is challenging, the majority of our understanding of stress and Alzheimer's comes from a large database of animal research. Beta-amyloid is a harmful peptide that forms plaques in the brain and surrounding blood vessels and is a main pathological characteristic of Alzheimer's disease.

Stress has been proven to enhance the development of harmful beta-amyloid in both acute and chronic stress animal models of Alzheimer's disease. This has also been linked to a faster decrease in cognition in these animal models when compared to controls. Early-life stress can also have long-term and irreversible impacts on these animals' brains, with significant increases in amyloid levels in the brain and cerebrospinal fluid (CSF).

Tau is the second important Alzheimer's protein. In Alzheimer's disease, tau tangles are the principal cause of neuronal death. Hyperphosphorylation of tau leads to the formation of tangles. Several studies have found that stress causes hyperphosphorylation of tau in animal models with pressure compared to those without stress.

Alzheimer's Disease Treatment and Stress

Given that stress exacerbates Alzheimer's pathogenesis in animal models, it's reasonable to anticipate that reducing stress levels would help to alleviate Alzheimer's pathology and symptoms in people.

In animal models, decreasing CRF levels by blocking CRF-receptors (CRFR1) resulted in lower overall levels of amyloidosis and plaques, as well as improved cognitive performance. Furthermore, glucocorticoid receptor inhibition has been linked to a reduction in Alzheimer's pathology in animal models, with clinical studies in a limited group of patients showing modest improvement in cognition. Clinical recovery, however, was minimal when compared to animal trials.

Unfortunately, several medications that appear to function well in mouse models do not appear to perform well in people, and some clinical studies have failed at Phase I or II stages. Although animal models are fundamental to the study of human health and illness, much research cannot be duplicated adequately during clinical trials due to species-specific characteristics and the higher complexity of all systems in humans. As a result, much more clinical research is needed before solid conclusions can be drawn on how stress impacts Alzheimer's disease and if anti-stress medicines may be utilized to treat the illness.

In conclusion, stress is not a major component in the genesis of Alzheimer's disease; rather, it may have a role in the illness's progression and worsening symptoms due to compromised immunological responses, which are significant in Alzheimer's disease. However, much more research on patients is needed before providing clinical recommendations.