Alzheimer’s at a young age

Alzheimer’s disease is characterized by a significant decline in memory and thinking functions and is also accompanied by difficulties in daily functioning. It usually begins in adults over the age of 65, with the prevalence of the disease increasing with age.

When the disease begins earlier, it is considered early-onset Alzheimer’s disease and is characterized by a somewhat different disease than classical Alzheimer’s.

There are often behavioral changes such as apathy, irritability, or responses that are not typical of that person’s character. There may also be changes in mood, such as anxiety or depression in the early stages, which often mask the memory difficulties.

There may be impairment in short-term memory, such as difficulty remembering appointments or events that occurred several days or months ago, what was eaten for breakfast, or what was said just minutes earlier. Another problem is impaired spatial orientation, with difficulty driving and confusion in places that were previously familiar. There may also be impaired orientation in time, such as difficulty remembering the date or day of the week. In some cases, there may also be a language disorder with changes in writing, difficulty retrieving words, and significant impairment in comprehension. Sometimes the patient is not aware of the severity of the condition, and then the difficulty is greater.

When there are several family members with Alzheimer’s disease, there is a higher suspicion of a genetic component. In Israel, genetic testing (for the APOE4 gene) is not routinely performed, except as part of research. This mutation increases the likelihood of developing Alzheimer’s disease at an older age.

There is also familial Alzheimer’s disease, which begins at a very young age, around 30–40, and several genes have been found to be responsible for it (APP, PSEN1, PSEN2). Mutations in these genes significantly increase the likelihood of developing the disease, but these mutations are uncommon.

There are several treatments given for Alzheimer’s disease. These are symptomatic medications (treating the symptoms only), which may slightly improve difficulties with concentration, alertness, or memory. They do not affect the course of the disease, and only some patients respond well to them. There is also an emphasis on the adaptation of the patient and the family to the new situation, with several interventions that have been found to be helpful, such as maintaining a varied daily routine, cognitive activity and physical activity, as well as occupational therapy.

The causes of the disease (at both younger and older ages) are not completely clear, but in addition to the genetic component, there is also a significant environmental component that has been found to be associated with the development of the disease. Therefore, there are additional treatment options beyond the conventional medication-based treatment. However, these environmental factors must be diagnosed (such as metals, chronic infections, and advanced nutritional deficiencies), as they are not reflected in the routine evaluation performed today. According to current research, lifestyle factors including cognitive activity, regular physical activity, and social activity, among others, also have a significant effect on a person’s brain function, whether or not they have the defective gene.

It is important to know that Alzheimer’s disease is a gradually progressive disease, and its signs in the brain occur a decade or two before symptoms appear. Therefore, it is very important to be evaluated as early as possible when there is a family history or concern about memory decline, or in order to understand how deterioration may be prevented, so that diagnosis and treatment can be provided in the best possible way.

References:

  1. Chia-Chen Liu, Takahisa Kanekiyo, Huaxi Xu, and Guojun Bu. Apolipoprotein E and Alzheimer disease: risk, mechanisms, and therapy. Nat Rev Neurol. 2013 Feb; 9(2): 106–118.
  2. N C Fox, E K Warrington, A L Seiffer, S K Agnew, M N Rossor. Presymptomatic cognitive deficits in individuals at risk of familial Alzheimer’s disease. A longitudinal prospective study. Brain, Volume 121, Issue 9, 1 September 1998, Pages 1631–1639.
  3. Dale E. Bredesen, Edwin C. Amos, Jonathan Canick, Mary Ackerley, Cyrus Raji, Milan Fiala, and Jamila Ahdidan. Reversal of cognitive decline in Alzheimer’s disease. Aging (Albany NY). 2016 Jun; 8(6): 1250–1258.
  4. Solomon A, Turunen H, Ngandu T, et al. Effect of the apolipoprotein E genotype on cognitive change during a multidomain lifestyle intervention: a subgroup analysis of a randomized clinical trial. JAMA Neurol. 2018 Jan 22.