The brains of people with Parkinson’s disease contain abnormal clumps of proteins called Lewy bodies. These clumps are largely made up of the protein alpha-synuclein, which plays a role in crosstalk between brain cells.

Since there are no membrane-bound organelles in prokaryotes, the ribosomes float free in the cytosol. Those floating ribosomes make proteins that will be used inside of the cell. Other ribosomes are found on the endoplasmic reticulum. Endoplasmic reticulum with attached ribosomes is called rough ER.

Ribosomes are found ‘free’ in the cytoplasm or bound to the endoplasmic reticulum (ER) to form rough ER. Several ribosomes can be attached to the same mRNA strand, this structure is called a polysome. Ribosomes have only a temporary existence.

Without mitochondria (singular, mitochondrion), higher animals would likely not exist because their cells would only be able to obtain energy from anaerobic respiration (in the absence of oxygen), a process much less efficient than aerobic respiration. …

Errors in protein synthesis disrupt cellular fitness, cause disease phenotypes, and shape gene and genome evolution.

Ingestion of diseased tissue (nerve tissue from mad cows) is known to be the cause of the prion disease. There is now evidence that other proteopathies can be induced by a similar mechanism, In all of these instances, an aberrant form of the protein itself appears to be the pathogenic agent.

The abnormal folding of the prion proteins leads to brain damage and the characteristic signs and symptoms of the disease. Prion diseases are usually rapidly progressive and always fatal.

AD is a proteopathy, neuropathologically characterized by accumulations of two proteins, amyloid beta (Aβ) and tau, against a background of progressive cortical atrophy resulting from the loss of neurons and synapses.

Tauopathies are neurodegenerative diseases with abundant filamentous inclusions made of microtubule-associated protein Tau in some nerve cells or in both nerve cells and glial cells.

Parkinson’s disease (PD) was not initially considered to be a typical tauopathy. However, recent studies have demonstrated increasing evidence of tau pathology in PD. A genome-wide association (GWA) study indicated a potential association between tauopathy and sporadic PD.

Both PSP and CBD are considered tauopathies because of the accumulation of tau protein in the brains, and MSA is considered a synucleinopathy owing to accumulation of α-synuclein. Although some pathological changes are found in both PSP and CBD, other changes allow the two conditions to be differentiated.

CTE is a tauopathy characterized by the deposition of hyperphosphorylated tau (p-tau) protein as neurofibrillary tangles, astrocytic tangles and neurites in striking clusters around small blood vessels of the cortex, typically at the sulcal depths. Severely affected cases show p-tau pathology throughout the brain.

It’s not reversible or curable. Mez says there can be no therapies to treat CTE until it can be diagnosed in living patients. However, some of the symptoms can be treated. For example, behavioral therapies can help treat mood changes.

Some researchers believe the severity of the disease might correlate with the length of time a person spend participating in the sport. Unfortunately, a 2009 analysis of 51 people who experience CTE found the average lifespan of those with the disease is just 51 years.

They divided CTE clinical presentations into three domains: behavioral/psychiatric, cognitive, and motor. The behavioral and psychiatric domain included aggression, depression, apathy, impulsivity, delusions including paranoia, and suicidality.

Can I get CTE from one concussion/hit to the head? We believe CTE is caused by repetitive brain trauma. This trauma includes both concussions that cause symptoms and subconcussive hits to the head that cause no symptoms.

CTE has been seen in people as young as 17, but symptoms do not generally begin appearing until years after the onset of head impacts.

Additionally, researchers found that most of the people studied with Stage IV also developed “a profound loss of attention and concentration, executive dysfunction, language difficulties, explosivity, aggressive tendencies, paranoia, depression, gait and visuospatial difficulties.”

Free ribosomes are located in the cytosol and are able to move throughout the cell, whereas fixed ribosomes are attached to the rER. Free ribosomes synthesize proteins that are released into the cytosol and used within the cell.

They are coded for by our genes and form the basis of living tissues. They also play a central role in biological processes. For example, proteins catalyse reactions in our bodies, transport molecules such as oxygen, keep us healthy as part of the immune system and transmit messages from cell to cell.

The best known forms of inducible proteopathy are prion diseases, which can be transmitted by exposure of a host organism to purified prion protein in a disease-causing conformation.

Alzheimer’s disease has been identified as a protein misfolding disease, or proteopathy, due to the accumulation of abnormally folded Amyloid-beta proteins in the brains of AD patients.

The beta-amyloid protein involved in Alzheimer’s comes in several different molecular forms that collect between neurons. It is formed from the breakdown of a larger protein, called amyloid precursor protein. One form, beta-amyloid 42, is thought to be especially toxic.

There’s no cure for Alzheimer’s, but one treatment may potentially delay decline from the disease, and there are drug and non-drug options that may help treat symptoms. Understanding available options can help individuals living with the disease and their caregivers to cope with symptoms and improve quality of life.

On average, people with Alzheimer’s disease live between three and 11 years after diagnosis, but some survive 20 years or more.

Finding a cure for neurodegenerative diseases such as Alzheimer’s is challenging. They’re difficult to diagnose, and drugs struggle to get into the brain as the brain’s blood supply is largely separate to the rest of the body. Not surprisingly, several companies have left this territory in recent years.

Aduhelm represents a first-of-its-kind treatment approved for Alzheimer’s disease. It is the first new treatment approved for Alzheimer’s since 2003 and is the first therapy that targets the fundamental pathophysiology of the disease.

Alzheimer’s disease and dementia are most common in Western Europe (with North America close behind) and least common in Sub-Saharan Africa. African-Americans are about twice as likely to have Alzheimer’s disease or other forms of dementia as whites.

There is currently no “cure” for dementia. In fact, because dementia is caused by different diseases it is unlikely that there will be a single cure for dementia. Research is aimed at finding cures for dementia-causing diseases, such as Alzheimer’s disease, frontotemporal dementia and dementia with Lewy bodies.

Similarly, dementia can be reversed if caught early enough and by attending to all the factors that affect brain function – including diet, exercise, stress, nutritional deficiencies, toxins, hormonal imbalances, and inflammation.

Several studies looking at the effect of aerobic exercise (exercise that increases your heart rate) in middle-aged or older adults have reported improvements in thinking and memory, and reduced rates of dementia.

The main risk factors for developing Alzheimer’s disease (AD) are age and gender. The incidence of the disease is higher in women than in men, and this cannot simply be attributed to the higher longevity of women versus men.